Dr Chen Chen Jiang

Dr Chen Chen Jiang

Cancer Institute NSW Career Development Fellow

School of Medicine and Public Health

Career Summary

Biography

Dr Chen Chen Jiang is a Cancer Institute NSW Career Development Fellow. She has been working on translational research in melanoma with a focused theme of “overcoming resistance of metastatic melanoma to treatment” for more than 10 years. She is currently in charge of the signal transduction team in the Melanoma Research Laboratory, which includes 3 research assistants and 3 PhD students.

Research support:  As a researcher still in the early/middle stage of her career, Dr Jiang as a chief investigator has received 1 NHMRC Project Grant ($341,175), 1 NHMRC Equipment Grant ($ 24,596) and 2 Cancer Council NSW Project Grants in the last five years ($718,500). As CIA, she received a Cure Cancer Australia Foundation Project Grant in 2010 ($90,000).  She was awarded an NHMRC training (postdoctoral) fellowship in 2011 ($320,032), and a highly competitive Cancer Institute NSW Career Development Fellowship in 2014 ($600,000).  In addition, she has received a number of competitive grants from other sources.

 

International and national standing:Dr Jiang’s work has resulted in 62 research publications in high impact journals including Nature Communications, PNAS, Cancer Research, Clinical Cancer Research, Autophagy, Oncogene, Cell Death and Differentiation and Cell Death and Diseases. Her career publications have attracted more than 1500 citations with H-index at 21 and Scopus H-index at18. 

 

Dr Jiang has served as a reviewer to assess grant applications for national and international funding bodies including NHMRC, the Cure Cancer Australia Foundation and the National Natural Science Fund of China. She was a Grant Review Committee member of Cancer Australia in 2014. 

Dr Jiang also serves as a regular reviewer for a number of journals including Clinical Cancer Research and Molecular Cancer Research.

She acted as the chair of the Scientific Program Committee of the Australian Society for Medical Research(ASMR)Satellite Scientific Meeting in Newcastle March 2014.

She was awarded the “Woman in Cancer Research Award” and the “Sanofi-Aventis Scholar-in-training Award” by the AACR in 2015 and 2010, respectively.

 

Collaborations:Dr Jiang has ongoing collaborations with a large number of researchers locally, nationally, and internationally. She has established productive collaborations with Prof Rodney Scott locally and Profs Richard Kefford and Richard Scolyer nationally. She has also established collaborations with researchers from many universities in China.  Her productive collaborations with researchers in China not only allows her to attract high quality students and visiting academics, but also enables her to apply for funding as a collaborator from various sources in China.

 

Supervision:In the last 5 years, Dr Jiang has supervised 5 PhD students and 8 visiting academics. All of these students and visiting academics have proven highly productive under her supervision, as evidenced by their awards for presentations at scientific conferences and their publications in high impact journals.

 

Professional involvment: Dr Jiang actively participates in activities of academic organisations. She is a member of AACR, the Australia and New Zealand Melanoma Trials Group, the Melanoma Tumour Group of the Hunter New England Area Health, and ASMR.

Community engagement and participation:Dr Jiang regularly presents her work to various community groups and writes newsletters for local medical research associations. Through collaboration with pharmaceutical companies, her research has contributed to the decision-making in planning and executing clinical trials with targeted inhibitors of the MAPK pathway.

 

Contribution to field of research: Dr Jiang pioneered studies on “understanding adaptive mechanisms of melanoma cells to endoplasmic reticulum (ER) stress”, which has provided a number of insights into resistance mechanisms of melanoma to apoptosis induced by ER stress. No one else has investigated ER stress in melanoma, and its effect on melanoma cell survival and responses to treatment, as systematically and as comprehensively as she has. She was also among the first to show that the inappropriate activation of survival pathways plays a critical role in the resistance of melanoma cells to apoptosis induced by various chemotherapeutic drugs. In addition, Dr Jiang was also among the first to show that MEK-independent mechanisms play an important role in resistance of melanoma cells to targeted inhibitors of mutant BRAF. More recently, she has become a leading figure in the investigation of the roles of microRNAs in the regulation of melanoma cell survival and proliferation.

 



Qualifications

  • PhD (Surgical Science), University of Newcastle
  • Bachelor of Medicine, Bengbu Medical College - China
  • Master of Applied Science (Biotechnology), University of Western Sydney

Keywords

  • Carcinogenesis
  • Oncology
  • cancer
  • cell death
  • overcome resistance of cancer cells to treatment
  • signal transduction

Languages

  • English (Fluent)
  • Mandarin (Mother)

Fields of Research

Code Description Percentage
111299 Oncology and Carcinogenesis not elsewhere classified 30
111201 Cancer Cell Biology 70

Professional Experience

UON Appointment

Title Organisation / Department
Cancer Institute NSW Career Development Fellow University of Newcastle
School of Medicine and Public Health
Australia
Casual Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Academic appointment

Dates Title Organisation / Department
1/06/2011 - 1/06/2015 Fellow - NHMRC University of Newcastle
School of Medicine and Public Health
Australia

Awards

Member

Year Award
2008 Runner-up of Student Poster award
Hunter Medical Research Institute (HMRI)

Prize

Year Award
2008 Best research showcase
Faculty of Health, University of Newcastle

Professional

Year Award
2015 AACR Woman in Cancer Research Award
American Association for Cancer Research (AACR)
2010 AACR Sanofi-Aventis Scholar-in-training Award
American Association for Cancer Research (AACR)

Invitations

Committee Member

Year Title / Rationale
2014 ASMR Satellite Scientific Meeting

Panel Participant

Year Title / Rationale
2015 Receptor-Interacting Protein Kinase 1 regulates survival of human melanoma cells upon endoplasmic reticulum stress through autophagy
2015 MicroRNA regulation of INPP4B to promote melanoma cell proliferation through PI3K/SGK3.
2015 Receptor-Interacting Protein Kinase 1 functions as an oncogenic regulator in human melanoma.
2013 Inhibition of oncogenic BRAF triggers immunogenic necrosis of human melanoma cells.
2013 PHLPP1 deactivates Akt and has a tumor suppressive role in human melanoma
2013 Co-targeting histone deacetylase inhibitor and oncogenic BRAF synergistically kill human melanoma cells by caspase-independent cell death
2010 Long-term exposure to the BRAFV600E inhibitor PLX4720 results in melanoma cells with increased activation of ERK1/2 and high proliferation potential.
2010 Transcriptional up-regulation of Mcl-1 by ETS1 down-stream of XBP-1 in melanoma cells upon ER stress

Participant

Year Title / Rationale
2012 PP2A signalling is overridden by MEK/ERK activity leading to suppression of Bim and progection of melanoma cells upon ER stress
2012 The cancer testis antigen MAGE-D2 protects human melanoma cells from TRAIL-induced apoptosis by suppressing TRAIL-R2 expression
2010 Adaptation to ER stress as a driver of increased expression of Mcl-1 with melanoma progression.
2010 Apoptosis response of mutant B-RAF human melanoma cells to a B-RAF inhibitor involves increased splicing production of BimS.

Prestigious works

Year Commenced Year Finished Prestigious Work Role
2014 2015 Member of The Australian Society for Medical Research (ASMR) member Member
2012 2015 The Melanoma Tumour Group of the Hunter New England Area Health Member Member
2010 2015 Member of The Australia and New Zealand Melanoma Trials Group (ANZMTG) member Member
2010 2015 Member of The Melanoma Institute of Australia (MIA) Member Member
2007 2015 Member of The American Association for Cancer Research (AACR) Member Member
2007 2015 Member of The Hunter Medical Research Institute (HMRI) member Member
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (91 outputs)

Year Citation Altmetrics Link
2017 Faulkner S, Jobling P, Rowe C, Rodriguez-Oliveira S, Roselli S, Thorne R, et al., 'Neurotrophin Receptors TrkA, p75(NTR), and Sortilin Are Increased and Targetable in Thyroid Cancer.', Am J Pathol, (2017)
DOI 10.1016/j.ajpath.2017.09.008
Co-authors Marjorie Walker, Xu Zhang, Christopher W Rowe Uon, Rick Thorne, Phillip Jobling, John Attia, Hubert Hondermarck, Christopher Oldmeadow
2017 Croft A, Guo ST, Sherwin S, Farrelly M, Yan XG, Zhang XD, Jiang CC, 'Functional identification of a novel transcript variant of INPP4B in human colon and breast cancer cells', Biochemical and Biophysical Research Communications, 485 47-53 (2017) [C1]

© 2017 Elsevier Inc. The 4-phosphatase Inositol polyphosphate 4-phosphatase II (INPP4B) is a regulator of the PI3K signalling pathway and functions to suppress or promote activat... [more]

© 2017 Elsevier Inc. The 4-phosphatase Inositol polyphosphate 4-phosphatase II (INPP4B) is a regulator of the PI3K signalling pathway and functions to suppress or promote activation of downstream kinases depending on cell type and context. Here we report the identification of a novel small transcript variant of INPP4B (INPP4B-S) that has a role in promoting proliferation of colon and breast cancer cells. INPP4B-S differed from full length INPP4B (INPP4B-FL) by the insertion of a small exon between exons 15 and 16 and the deletion of exons 20¿24. Nevertheless, INPP4B-S retained all the functional domains of INPP4B-FL and was similarly located to the cytoplasm. Overexpression of INPP4B-S increased, whereas selective knockdown of INPP4B-S reduced the rate of proliferation in HCT116 and MCF-7¿cells. These results warrant further investigation of the role INPP4B-S in activation of downstream kinases and in regulation of cancer pathogenesis.

DOI 10.1016/j.bbrc.2017.02.012
Co-authors Xu Zhang
2017 Guo ST, Guo XY, Wang J, Wang CY, Yang RH, Wang FH, et al., 'MicroRNA-645 is an oncogenic regulator in colon cancer', ONCOGENESIS, 6 (2017) [C1]
DOI 10.1038/oncsis.2017.37
Citations Web of Science - 1
Co-authors Xu Zhang, Rick Thorne, Hubert Hondermarck, Lei Jin
2017 Zhou C, Song L, Zhang Z, Pan Q, Chen Y, Liu L, et al., '3-Bromopyruvate enhances TRAIL-induced apoptosis in human nasopharyngeal carcinoma cells through CHOP-dependent upregulation of TRAIL-R2', ANTI-CANCER DRUGS, 28 739-749 (2017)
DOI 10.1097/CAD.0000000000000502
2017 Liu F, Jiang CC, Yan XG, Tseng H-Y, Wang CY, Zhang YY, et al., 'BRAF/MEK inhibitors promote CD47 expression that is reversible by ERK inhibition in melanoma.', Oncotarget, 8 69477-69492 (2017) [C1]
DOI 10.18632/oncotarget.17704
Co-authors Xu Zhang, Lei Jin, Rick Thorne
2017 Wang CY, Guo ST, Croft A, Yan XG, Jin L, Zhang XD, Jiang CC, 'BAG3-dependent expression of Mcl-1 confers resistance of mutant KRAS colon cancer cells to the HSP90 inhibitor AUY922.', Mol Carcinog, (2017)
DOI 10.1002/mc.22755
Co-authors Xu Zhang
2017 Liu F, Jiang CC, Yan XG, Tseng H-Y, Wang CY, Zhang YY, et al., 'BRAF/MEK inhibitors promote CD47 expression that is reversible by ERK inhibition in melanoma.', Oncotarget, 8 69477-69492 (2017) [C1]
DOI 10.18632/oncotarget.17704
Co-authors Xu Zhang, Lei Jin, Rick Thorne
2016 Chen J, Jiang CC, Jin L, Zhang XD, 'Regulation of PD-L1: A novel role of pro-survival signalling in cancer', Annals of Oncology, 27 409-416 (2016) [C1]

© The Author 2015. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. Evasion of immune system is a hallmark of can... [more]

© The Author 2015. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. Evasion of immune system is a hallmark of cancer, which enables cancer cells to escape the attack from immune cells. Cancer cells can express many immune inhibitory signalling proteins to cause immune cell dysfunction and apoptosis. One of these inhibitory molecules is programmed death-ligand-1 (PD-L1), which binds to programmed death-1 (PD-1) expressed on T-cells, B-cells, dendritic cells and natural killer T-cells to suppress anti-cancer immunity. Therefore, anti-PD-L1 and anti-PD-1 antibodies have been used for the treatment of cancer, showing promising outcomes. However, only a proportion of patients respond to the treatments. Further understanding of the regulation of PD-L1 expression could be helpful for the improvement of anti-PD-L1 and anti-PD-1 treatments. Studies have shown that PD-L1 expression is regulated by signalling pathways, transcriptional factors and epigenetic factors. In this review, we summarise the recent progress of the regulation of PD-L1 expression in cancer cells and propose a regulatory model for unified explanation. Both PI3K and MAPK pathways are involved in PD-L1 regulation but the downstream molecules that control PD-L1 and cell proliferation may differ. Transcriptional factors hypoxia-inducible factor-1a and signal transducer and activation of transcription-3 act on the promoter of PD-L1 to regulate its expression. In addition, microRNAs including miR-570, miR-513, miR-197, miR-34a and miR-200 negatively regulate PD-L1. Clinically, it could increase treatment efficacy of targeted therapy by choosing those molecules that control both PD-L1 expression and cell proliferation.

DOI 10.1093/annonc/mdv615
Citations Scopus - 61Web of Science - 60
Co-authors Lei Jin, Xu Zhang
2016 Yanwang C, Guo ST, Yuwang J, Liu F, Zhang YY, Yari H, et al., 'Inhibition of HSP90 by AUY922 preferentially kills mutantkrascolon cancer cellsbyactivatingbim through ER stress', Molecular Cancer Therapeutics, 15 448-459 (2016) [C1]

© 2016 American Association for Cancer Research. Oncogenic mutations of KRAS pose a great challenge in the treatment of colorectal cancer. Here we report that mutant KRAS colon c... [more]

© 2016 American Association for Cancer Research. Oncogenic mutations of KRAS pose a great challenge in the treatment of colorectal cancer. Here we report that mutant KRAS colon cancer cells are nevertheless more susceptible to apoptosis induced by the HSP90 inhibitor AUY922 than those carrying wild-type KRAS. Although AUY922 inhibited HSP90 activity with comparable potency in colon cancer cells irrespective of their KRAS mutational statuses, those with mutant KRAS were markedly more sensitive to AUY922-induced apoptosis. This was associated with upregulation of the BH3-only proteins Bim, Bik, and PUMA.However, only Bim appeared essential, in that knockdown of Bim abolished, whereas knockdown of Bik or PUMA only moderately attenuated apoptosis induced by AUY922. Mechanistic investigations revealed that endoplasmic reticulum (ER) stress was responsible for AUY922-induced upregulation of Bim, which was inhibited by a chemical chaperone or overexpression of GRP78. Conversely, siRNA knockdown of GRP78 or XBP-1 enhanced AUY922-induced apoptosis. Remarkably, AUY922 inhibited the growth of mutant KRAS colon cancer xenografts through activation of Bim that was similarly associated with ER stress. Taken together, these results suggest that AUY922 is a promising drug in the treatment of mutant KRAS colon cancers, and the agents that enhance the apoptosis-inducing potential of Bimmaybe useful to improve the therapeutic efficacy.

DOI 10.1158/1535-7163.MCT-15-0778
Citations Scopus - 4Web of Science - 2
Co-authors Xu Zhang, Lei Jin
2016 Huang YY, Pu LJ, Song LL, Ma LY, Liu H, Jiang CC, 'Knockdown of GRP78 enhances cell death by cisplatin and radiotherapy in nasopharyngeal cells', Anti-Cancer Drugs, 27 726-733 (2016) [C1]

© Copyright 2016 Wolters Kluwer Health, Inc. All rights reserved. Radiotherapy and adjuvant cisplatin chemotherapy are the mainstream approaches in the treatment of nasopharyngea... [more]

© Copyright 2016 Wolters Kluwer Health, Inc. All rights reserved. Radiotherapy and adjuvant cisplatin chemotherapy are the mainstream approaches in the treatment of nasopharyngeal carcinoma (NPC). These have been shown to effectively improve the outcome and reduce tumor recurrence. However, radiotherapy and chemotherapy resistance during the course of treatment has become more common recently, resulting in the failure of NPC therapy. Therefore, new therapeutic strategies or adjuvant drugs are urgently needed. The current study was designed to look for new treatment strategies or auxiliary drugs in the treatment of NPC. Two human NPC cell lines, HNE1 and HNE1/DDP, were used to examine the relationship between endoplasmic reticulum stress and cell resistance to ionizing radiation (IR) and cisplatin (DDP). Cell proliferation was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Meanwhile, propidium iodide (PI) staining and PI/Annexin V staining were used to observe cell apoptosis. Finally, western blot was used to detect the endogenous expression of glucose-regulated protein 78 (GRP78) and other apoptosis-related proteins. GRP78 small interference RNA was transfected using Lipofectamine 2000. Compared with HNE1/DDP, IR and DDP increased the cell apoptosis and inhibited the cell proliferation of HNE1. Inhibition of GRP78 can reverse IR and DDP resistance in NPC cells by PI/Annexin V staining. Knockdown of GRP78 upregulates the expression of pro-apoptotic proteins and downregulates the expression of antiapoptotic proteins. These results indicate that HNE1 is more sensitive to DDP and IR than HNE1/DDP. Knockdown GRP78 can reverse IR and DDP resistance in NPC cells. Inhibition of GRP78 gives us a new target to overcome resistance to radiotherapy and chemotherapy of NPC cells. Thus, this study should be further explored in vivo and assessed for possible clinical applications.

DOI 10.1097/CAD.0000000000000377
2016 Wang JY, Jin L, Yan XG, Sherwin S, Farrelly M, Zhang YY, et al., 'Reactive Oxygen Species Dictate the Apoptotic Response of Melanoma Cells to¿TH588', Journal of Investigative Dermatology, 136 2277-2286 (2016) [C1]

© 2016 The Authors The effect of MTH1 inhibition on cancer cell survival has been elusive. Here we report that although silencing of MTH1 does not affect survival of melanoma cel... [more]

© 2016 The Authors The effect of MTH1 inhibition on cancer cell survival has been elusive. Here we report that although silencing of MTH1 does not affect survival of melanoma cells, TH588, one of the first-in-class MTH1 inhibitors, kills melanoma cells through apoptosis independently of its inhibitory effect on MTH1. Induction of apoptosis by TH588 was not alleviated by MTH1 overexpression or introduction of the bacterial homolog of MTH1 that has 8-oxodGTPase activity but cannot be inhibited by TH588, indicating that MTH1 inhibition is not the cause of TH588-induced killing of melanoma cells. Although knockdown of MTH1 did not impinge on the viability of melanoma cells, it rendered melanoma cells sensitive to apoptosis induced by the oxidative stress inducer elesclomol. Of note, treatment with elesclomol also enhanced TH588-induced apoptosis, whereas a reactive oxygen species scavenger or an antioxidant attenuated the apoptosis triggered by TH588. Indeed, the sensitivity of melanoma cells to TH588 was correlated with endogenous levels of reactive oxygen species. Collectively, these results indicate that the cytotoxicity of TH588 toward melanoma cells is not associated with its inhibitory effect on MTH1, although it is mediated by cellular production of ROS.

DOI 10.1016/j.jid.2016.06.625
Citations Scopus - 3Web of Science - 1
Co-authors Lei Jin, Xu Zhang
2016 Wang CY, Guo ST, Wang JY, Yan XG, Farrelly M, Zhang YY, et al., 'Reactivation of ERK and Akt confers resistance of mutant BRAF colon cancer cells to the HSP90 inhibitor AUY922', Oncotarget, 7 49597-49610 (2016) [C1]

Oncogenic mutations of BRAF occur in approximately 10% of colon cancers and are associated with their resistance to clinically available therapeutic drugs and poor prognosis of th... [more]

Oncogenic mutations of BRAF occur in approximately 10% of colon cancers and are associated with their resistance to clinically available therapeutic drugs and poor prognosis of the patients. Here we report that colon cancer cells with mutant BRAF are also resistant to the heat shock protein 90 (HSP90) inhibitor AUY922, and that this is caused by rebound activation of ERK and Akt. Although AUY922 triggered rapid reduction in ERK and Akt activation in both wild-type and mutant BRAF colon cancer cells, activation of ERK and Akt rebounded shortly in the latter leading to resistance of the cells to AUY922-induced apoptosis. Reactivation of ERK was associated with the persistent expression of mutant BRAF, which, despite being a client of HSP90, was only partially degraded by AUY922, whereas reactivation of Akt was related to the activity of the HSP90 co-chaperone, cell division cycle 37 (CDC37), in that knockdown of CDC37 inhibited Akt reactivation in mutant colon cancer cells treated with AUY922. In support, as a HSP90 client protein, Akt was only diminished by AUY922 in wild-type but not mutant BRAF colon cancer cells. Collectively, these results reveal that reactivation of ERK and Akt associated respectively with the activity of mutant BRAF and CDC37 renders mutant BRAF colon cancer cells resistant to AUY922, with implications of co-targeting mutant BRAF and/or CDC37 and HSP90 in the treatment of mutant BRAF colon cancers.

DOI 10.18632/oncotarget.10414
Citations Scopus - 3Web of Science - 1
Co-authors Xu Zhang, Lei Jin
2016 Zhang P, Hong H, Sun X, Jiang H, Ma S, Zhao S, et al., 'MicroRNA-10b regulates epithelial-mesenchymal transition by modulating KLF4/Notch1/E-cadherin in cisplatin-resistant nasopharyngeal carcinoma cells.', Am J Cancer Res, 6 141-156 (2016) [C1]
Citations Web of Science - 8
2016 Song L, Ma L, Chen G, Huang Y, Sun X, Jiang C, Liu H, 'Autophagy inhibitor 3-methyladenine enhances the sensitivity of nasopharyngeal carcinoma cells to chemotherapy and radiotherapy', Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences, 41 9-18 (2016)

Abstract available from the publisher.... [more]

Abstract available from the publisher.

DOI 10.11817/j.issn.1672-7347.2016.01.002
Citations Scopus - 3
2016 Zhang P, Hong H, Sun X, Jiang H, Ma S, Zhao S, et al., 'MicroRNA-10b regulates epithelial-mesenchymal transition by modulating KLF4/Notch1/E-cadherin in cisplatin-resistant nasopharyngeal carcinoma cells', American Journal of Cancer Research, 6 425-439 (2016)

Epithelial-mesenchymal transition (EMT) is an initiating event in tumor cell invasion and metastasis that contributes to therapeutic resistance to compounds including cisplatin. M... [more]

Epithelial-mesenchymal transition (EMT) is an initiating event in tumor cell invasion and metastasis that contributes to therapeutic resistance to compounds including cisplatin. MicroRNAs (miRNAs) have been associated with EMT as well as resistance to standard therapies. However, the underlying mechanisms by which miRNAs control the development of resistance to cisplatin (DDP), and the accompanying EMT-like properties are required to elucidate. Here we show that microRNA-10b (miR-10b) is up-regulated in HNE1/DDP cells, and inhibition of miR-10b expression reversed the EMT phenotype. However, over-expression of miR-10b was able to promote the acquisition of an EMT phenotype in HNE1 cells. Additionally, we identified that miR-10b expression inversely correlates with KLF4, which then controls expression of Notch1. Knock-down of Notch1 inhibited cell migration, invasion, and reversed EMT in HNE1/DDP cells, which was dependent on miR-10b. In summary, our results reveal that miR-10b regulates EMT by modulating KLF4/Notch1/E-cadherin expression, which promotes invasion and migration of nasal pharyngeal carcinoma cells.

Citations Scopus - 8
2016 Jiang CC, Croft A, Tseng HY, Guo ST, Jin L, Hersey P, Zhang XD, 'Repression of microRNA-768-3p by MEK/ERK signalling contributes to enhanced mRNA translation in human melanoma', Oncogene, (2016)
DOI 10.1038/onc.2016.144
Co-authors Lei Jin, Xu Zhang
2016 Jin L, Chen J, Liu XY, Jiang C, Zhang XD, 'The double life of RIPK1', Molecular & Cellular Oncology,, 3 (2016)
DOI 10.1080/23723556.2015.1035690
Citations Web of Science - 1
Co-authors Xu Zhang, Lei Jin
2016 Guo ST, Chi MN, Yang RH, Guo XY, Zan LK, Wang CY, et al., 'INPP4B is an oncogenic regulator in human colon cancer', Oncogene, 35 3049-3061 (2016) [C1]

© 2016 Macmillan Publishers Limited. All rights reserved. Inositol polyphosphate 4-phosphatase type II (INPP4B) negatively regulates phosphatidylinositol 3-kinase signaling and i... [more]

© 2016 Macmillan Publishers Limited. All rights reserved. Inositol polyphosphate 4-phosphatase type II (INPP4B) negatively regulates phosphatidylinositol 3-kinase signaling and is a tumor suppressor in some types of cancers. However, we have found that it is frequently upregulated in human colon cancer cells. Here we show that silencing of INPP4B blocks activation of Akt and serum-and glucocorticoid-regulated kinase 3 (SGK3), inhibits colon cancer cell proliferation and retards colon cancer xenograft growth. Conversely, overexpression of INPP4B increases proliferation and triggers anchorage-independent growth of normal colon epithelial cells. Moreover, we demonstrate that the effect of INPP4B on Akt and SGK3 is associated with inactivation of phosphate and tensin homolog through its protein phosphatase activity and that the increase in INPP4B is due to Ets-1-mediated transcriptional upregulation in colon cancer cells. Collectively, these results suggest that INPP4B may function as an oncogenic driver in colon cancer, with potential implications for targeting INPP4B as a novel approach to treat this disease.

DOI 10.1038/onc.2015.361
Citations Scopus - 7Web of Science - 8
Co-authors Lei Jin, Stephen Ackland, Xu Zhang, Rick Thorne, Hubert Hondermarck, Rodney Scott
2015 Roselli S, Pundavela J, Demont Y, Faulkner S, Keene S, Attia J, et al., 'Sortilin is associated with breast cancer aggressiveness and contributes to tumor cell adhesion and invasion', Oncotarget, 6 10473-10486 (2015) [C1]

The neuronal membrane protein sortilin has been reported in a few cancer cell lines, but its expression and impact in human tumors is unclear. In this study, sortilin was analyzed... [more]

The neuronal membrane protein sortilin has been reported in a few cancer cell lines, but its expression and impact in human tumors is unclear. In this study, sortilin was analyzed by immunohistochemistry in a series of 318 clinically annotated breast cancers and 53 normal breast tissues. Sortilin was detected in epithelial cells, with increased levels in cancers, as compared to normal tissues (p = 0.0088). It was found in 79% of invasive ductal carcinomas and 54% of invasive lobular carcinomas (p < 0.0001). There was an association between sortilin expression and lymph node involvement (p = 0.0093), suggesting a relationship with metastatic potential. In cell culture, sortilin levels were higher in cancer cell lines compared to non-tumorigenic breast epithelial cells and siRNA knockdown of sortilin inhibited cancer cell adhesion, while proliferation and apoptosis were not affected. Breast cancer cell migration and invasion were also inhibited by sortilin knockdown, with a decrease in focal adhesion kinase and SRC phosphorylation. In conclusion, sortilin participates in breast tumor aggressiveness and may constitute a new therapeutic target against tumor cell invasion.

Citations Scopus - 5Web of Science - 6
Co-authors Hubert Hondermarck, Xu Zhang, John Attia, Marjorie Walker
2015 Tay KH, Liu X, Chi M, Jin L, Jiang CC, Guo ST, et al., 'Involvement of vacuolar H

© 2014 John Wiley &amp; Sons A/S. Targeting the sphingosine 1-phosphate (S1P)/S1P receptor (S1PR) signalling axis is emerging as a promising strategy in the treatment of cancer... [more]

© 2014 John Wiley & Sons A/S. Targeting the sphingosine 1-phosphate (S1P)/S1P receptor (S1PR) signalling axis is emerging as a promising strategy in the treatment of cancer. However, the effect of such an approach on survival of human melanoma cells remains less understood. Here, we show that the sphingosine analogue FTY720 that functionally antagonises S1PRs kills human melanoma cells through a mechanism involving the vacuolar H + -ATPase activity. Moreover, we demonstrate that FTY720-triggered cell death is characterized by features of necrosis and is not dependent on receptor-interacting protein kinase 1 or lysosome cathepsins, nor was it associated with the activation of protein phosphatase 2A. Instead, it is mediated by increased production of reactive oxygen species and is antagonized by activation of autophagy. Collectively, these results suggest that FTY720 and its analogues are promising candidates for further development as new therapeutic agents in the treatment of melanoma.

DOI 10.1111/pcmr.12326
Citations Scopus - 6Web of Science - 6
Co-authors Nikki Verrills, Lei Jin, Xu Zhang
2015 Luan Q, Jin L, Jiang CC, Tay KH, Lai F, Liu XY, et al., 'RIPK1 regulates survival of human melanoma cells upon endoplasmic reticulum stress through autophagy.', Autophagy, 11 975-994 (2015) [C1]
DOI 10.1080/15548627.2015.1049800
Citations Scopus - 12Web of Science - 11
Co-authors Xu Zhang, Lei Jin
2015 Sun Y, Liu Z, Zou X, Lan Y, Sun X, Wang X, et al., 'Mechanisms underlying 3-bromopyruvate-induced cell death in colon cancer', JOURNAL OF BIOENERGETICS AND BIOMEMBRANES, 47 319-329 (2015) [C1]
DOI 10.1007/s10863-015-9612-1
Citations Scopus - 7Web of Science - 7
2015 Jiang C, Chi MN, Guo ST, Wilmott JS, Guo X Y, Yan X G, et al., 'INPP4B is upregulated and functions as an oncogenic driver through SGK3 in a subset of melanomas', Oncotarget, 6 39891-39907 (2015) [C1]
DOI 10.18632/oncotarget.5359
Citations Scopus - 13Web of Science - 10
Co-authors Hubert Hondermarck, Xu Zhang, Lei Jin
2015 Liu Z, Sun Y, Hong H, Zhao S, Zou X, Ma R, et al., '3-bromopyruvate enhanced daunorubicin-induced cytotoxicity involved in monocarboxylate transporter 1 in breast cancer cells', AMERICAN JOURNAL OF CANCER RESEARCH, 5 2673-2685 (2015)
Citations Scopus - 5Web of Science - 5
2015 Zhao S, Li H, Jiang C, Ma T, Wu C, Huo Q, Liu H, '17-Demethoxy-reblastatin, an Hsp90 inhibitor, induces mitochondria-mediated apoptosis through downregulation of Mcl-1 in human hepatocellular carcinoma cells', JOURNAL OF BIOENERGETICS AND BIOMEMBRANES, 47 373-381 (2015) [C1]
DOI 10.1007/s10863-015-9620-1
Citations Scopus - 5Web of Science - 3
2015 Liu XY, Lai F, Yan XG, Jiang CC, Guo ST, Wang CY, et al., 'RIP1 kinase is an oncogenic driver in melanoma', Cancer Research, 75 1736-1748 (2015) [C1]

© 2015 AACR. Although many studies have uncovered an important role for the receptor-binding protein kinase RIP1 in controlling cell death signaling, its possible contributions t... [more]

© 2015 AACR. Although many studies have uncovered an important role for the receptor-binding protein kinase RIP1 in controlling cell death signaling, its possible contributions to cancer pathogenesis have been little explored. Here, we report that RIP1 functions as an oncogenic driver in human melanoma. Although RIP1 was commonly upregulated in melanoma, RIP1 silencing inhibited melanoma cell proliferation in vitro and retarded the growth of melanoma xenografts in vivo. Conversely, while inducing apoptosis in a small proportion of melanoma cells, RIP1 overexpression enhanced proliferation in the remaining cells. Mechanistic investigations revealed that the proliferative effects of RIP1 overexpression were mediated by NF-¿B activation. Strikingly, ectopic expression of RIP1 enhanced the proliferation of primary melanocytes, triggering their anchorageindependent cell growth in an NF-¿B-dependent manner. We identified DNA copy-number gain and constitutive ubiquitination by a TNFa autocrine loop mechanism as two mechanisms of RIP1 upregulation in human melanomas. Collectively, our findings define RIP1 as an oncogenic driver in melanoma, with potential implications for targeting its NF-¿B-dependent activation mechanism as a novel approach to treat this disease.

DOI 10.1158/0008-5472.CAN-14-2199
Citations Scopus - 12Web of Science - 12
Co-authors Xu Zhang, Lei Jin
2015 Zou X, Zhang M, Sun Y, Zhao S, Wei Y, Zhang X, et al., 'Inhibitory effects of 3-bromopyruvate in human nasopharyngeal carcinoma cells', ONCOLOGY REPORTS, 34 1895-1904 (2015) [C1]
DOI 10.3892/or.2015.4147
Citations Scopus - 6Web of Science - 6
Co-authors Xu Zhang
2014 Dong L, Jin L, Tseng HY, Wang CY, Wilmott JS, Yosufi B, et al., 'Oncogenic suppression of PHLPP1 in human melanoma', Oncogene, 33 4756-4766 (2014)

© 2014 Macmillan Publishers Limited. Akt is constitutively activated in up to 70% of human melanomas and has an important role in the pathogenesis of the disease. However, little... [more]

© 2014 Macmillan Publishers Limited. Akt is constitutively activated in up to 70% of human melanomas and has an important role in the pathogenesis of the disease. However, little is known about protein phosphatases that dephosphorylate and thereby inactivate it in melanoma cells. Here we report that suppression of pleckstrin homology domain and leucine-rich repeat Ser/Thr protein phosphatase 1 (PHLPP1) by DNA methylation promotes Akt activation and has an oncogenic role in melanoma. While it is commonly downregulated, overexpression of PHLPP1 reduces Akt activation and inhibits melanoma cell proliferation in vitro, and retards melanoma growth in a xenograft model. In contrast, knockdown of PHLPP1 increases Akt activation, enhances melanoma cell and melanocyte proliferation, and results in anchorage-independent growth of melanocytes. Suppression of PHLPP1 involves blockade of binding of the transcription factor Sp1 to the PHLPP1 promoter. Collectively, these results suggest that suppression of PHLPP1 by DNA methylation contributes to melanoma development and progression.

DOI 10.1038/onc.2013.420
Citations Scopus - 6
Co-authors Lei Jin, Xu Zhang
2014 Liu YL, Lai F, Wilmott JS, Yan XG, Liu XY, Luan Q, et al., 'Noxa upregulation by oncogenic activation of MEK/ERK through CREB promotes autophagy in human melanoma cells', Oncotarget, 5 11237-11251 (2014) [C1]

Reduction in the expression of the anti-survival BH3-only proteins PUMA and Bim is associated with the pathogenesis of melanoma. However, we have found that the expression of the ... [more]

Reduction in the expression of the anti-survival BH3-only proteins PUMA and Bim is associated with the pathogenesis of melanoma. However, we have found that the expression of the other BH3-only protein Noxa is commonly upregulated in melanoma cells, and that this is driven by oncogenic activation of MEK/ERK. Immunohistochemistry studies showed that Noxa was expressed at higher levels in melanomas than nevi. Moreover, the expression of Noxa was increased in metastatic compared to primary melanomas, and in thick primaries compared to thin primaries. Inhibition of oncogenic BRAF V600E or MEK downregulated Noxa, whereas activation of MEK/ERK caused its upregulation. In addition, introduction of BRAFV600E increased Noxa expression in melanocytes. Upregulation of Noxa was due to a transcriptional increase mediated by cAMP responsive element binding protein, activation of which was also increased by MEK/ERK signaling in melanoma cells. Significantly, Noxa appeared necessary for constitutive activation of autophagy, albeit at low levels, by MEK/ERK in melanoma cells. Furthermore, it was required for autophagy activation that delayed apoptosis in melanoma cells undergoing nutrient deprivation. These results reveal that oncogenic activation of MEK/ERK drives Noxa expression to promote autophagy, and suggest that Noxa has an indirect anti-apoptosis role in melanoma cells under nutrient starvation conditions.

Citations Scopus - 16Web of Science - 16
Co-authors Xu Zhang, Lei Jin
2014 Zhang Q, Zhang Y, Zhang P, Chao Z, Xia F, Jiang C, et al., 'Hexokinase II inhibitor, 3-BrPA induced autophagy by stimulating ROS formation in human breast cancer cells', Genes and Cancer, 5 100-112 (2014)

© 2014, Impact Journals LLC. All Rights Reserved. Hexokinase II (HKII), a key enzyme of glycolysis, is widely over-expressed in cancer cells. 3-bromopyruvate (3-BrPA), an inhibit... [more]

© 2014, Impact Journals LLC. All Rights Reserved. Hexokinase II (HKII), a key enzyme of glycolysis, is widely over-expressed in cancer cells. 3-bromopyruvate (3-BrPA), an inhibitor of HK II, has been proposed as a specific antitumor agent. Autophagy is a process that regulates the balance between protein synthesis and protein degradation. Autophagy in mammalian systems occurs under basal conditions and can be stimulated by stresses, including starvation, oxidative stress. Therefore, we hypothesized that 3-BrPA could induce autophagy. In the present study, we explored the mechanism of 3-BrPA and its combined action with chloroquine. Our results demonstrate that in MDA-MB-435 and in MDA-MB-231 cells, 3-BrPA induces autophagy, which can be inhibited by chloroquine. Furthermore, the combined treatment synergistically decreased the number of viable cells. Interesti ngly, the combined treatment triggered apoptosis in MDA-MB-435 cells, while it induced necroptosis in MDA-MB-231 cells. ROS mediated cell death when 3-BrPA and CQ were co-administered. Finally, CQ enhanced the anticancer efficacy of 3-BrPA in vivo. Collectively, our results show that 3-BrPA triggers autophagy, increasing breast cancer cell resistance to 3-BrPA treatment and that CQ enhanced 3-BrPA-induced cell death in breast cancer cells by stimulating ROS formation. Thus, inhibition of autophagy may be an innovative strategy for adjuvant chemotherapy of breast cancer

Citations Scopus - 18
Co-authors Xu Zhang
2014 Cheng X, Liu H, Jiang C-C, Fang L, Chen C, Zhang X-D, Jiang Z-W, 'Connecting endoplasmic reticulum stress to autophagy through IRE1/JNK/beclin-1 in breast cancer cells.', Int J Mol Med, 34 772-781 (2014)
DOI 10.3892/ijmm.2014.1822
Citations Scopus - 21
Co-authors Xu Zhang
2014 Croft A, Tay KH, Boyd SC, Guo ST, Jiang CC, Lai F, et al., 'Oncogenic activation of MEK/ERK primes melanoma cells for adaptation to endoplasmic reticulum stress', Journal of Investigative Dermatology, 134 488-497 (2014) [C1]

Cancer cells commonly undergo chronic endoplasmic reticulum (ER) stress, to which the cells have to adapt for survival and proliferation. We report here that in melanoma cells int... [more]

Cancer cells commonly undergo chronic endoplasmic reticulum (ER) stress, to which the cells have to adapt for survival and proliferation. We report here that in melanoma cells intrinsic activation of the ER stress response/unfolded protein response (UPR) is, at least in part, caused by increased outputs of protein synthesis driven by oncogenic activation of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK) and promotes proliferation and protects against apoptosis induced by acute ER stress. Inhibition of oncogenic BRAF V600E or MEK-attenuated activation of inositol-requiring enzyme 1 (IRE1) and activating transcription factor 6 (ATF6) signaling of the UPR in melanoma cells. This was associated with decreased phosphorylation of eukaryotic initiation factor 4E (eIF4E) and nascent protein synthesis and was recapitulated by knockdown of eIF4E. In line with this, introduction of BRAF V600E into melanocytes led to increases in eIF4E phosphorylation and protein production and triggered activation of the UPR. Similar to knockdown of glucose-regulated protein 78 (GRP78), inhibition of XBP1 decelerated melanoma cell proliferation and enhanced apoptosis induced by the pharmacological ER stress inducers tunicamycin and thapasigargin. Collectively, these results reveal that potentiation of adaptation to chronic ER stress is another mechanism by which oncogenic activation of the MEK/ERK pathway promotes the pathogenesis of melanoma. © 2014 The Society for Investigative Dermatology.

DOI 10.1038/jid.2013.325
Citations Scopus - 30Web of Science - 27
Co-authors Xu Zhang, Lei Jin
2014 Chao ZH, Zhao SR, Jiang CC, Zhang QW, Li Y, Liu H, Jiang ZW, 'The establishment and evaluation of breast cancer cells in C
DOI 10.3969/j.issn.1001-1978.2014.02.033
2014 Zhang Q, Gan H, Cheng Z, Zhao S, Chen C, Jiang C, et al., '[2-Deoxy-D-glucose combined with Taxol inhibits VEGF expression and induces apoptosis in orthotopically transplanted breast cancer in C3H mice]', Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 34 193-196 (2014)

OBJECTIVE: To investigate the antineoplastic effects of 2-Deoxy-D-glucose (2-DG) combined with Taxol on orthotopically transplanted breast cancer in C3H mice and explore the mecha... [more]

OBJECTIVE: To investigate the antineoplastic effects of 2-Deoxy-D-glucose (2-DG) combined with Taxol on orthotopically transplanted breast cancer in C3H mice and explore the mechanism. METHODS: C3H mice bearing orthotopically transplanted breast cancer xenograft were randomly divided into 4 groups, namely the control group, 2-DG group, Taxol group, and 2-DG+Taxol group. The corresponding drugs were administered intraperitoneally every 3 days for 18 consecutive days, and the tumor volume was measured every 3 days to draw the tumor growth curve. The mice were then sacrificed to measure the tumor weight on day 19 and examine tumor cell apoptosis with TUNEL assay and VEGF expression using immunohistochemistry. RESULTS: 2-DG combined with Taxol obviously suppressed the tumor growth with a tumor inhibition rate of 66.06% as compared to the rate of 36.97% in Taxol group. The combined treatment also caused more obvious cell apoptosis and significantly reduced VEGF expression in the tumor cells as compared with the other groups. CONCLUSION: 2-DG can enhance the inhibitory effect of Taxol on orthotopically transplanted breast cancer xenograft in C3H mice probably by inducing tumor cell apoptosis and lowering VEGF expressions.

Citations Scopus - 1
2014 Zhao RS, Zhang YY, Wu CZ, Li HM, Jiang C, Jiang ZW, Liu H, '3-bromopyruvate enhances cisplatin sensitivity of hepatocellular carcinoma cells in vitro.', Nan Fang Yi Ke Da Xue Xue Bao = Journal of Southern Medical University, 34 25-30 (2014) [C1]
2014 Dong L, Jin L, Tseng HY, Wang CY, Wilmott JS, Yosufi B, et al., 'Oncogenic suppression of PHLPP1 in human melanoma', Oncogene, 33 4756-4766 (2014) [C1]

© 2014 Macmillan Publishers Limited. Akt is constitutively activated in up to 70% of human melanomas and has an important role in the pathogenesis of the disease. However, little... [more]

© 2014 Macmillan Publishers Limited. Akt is constitutively activated in up to 70% of human melanomas and has an important role in the pathogenesis of the disease. However, little is known about protein phosphatases that dephosphorylate and thereby inactivate it in melanoma cells. Here we report that suppression of pleckstrin homology domain and leucine-rich repeat Ser/Thr protein phosphatase 1 (PHLPP1) by DNA methylation promotes Akt activation and has an oncogenic role in melanoma. While it is commonly downregulated, overexpression of PHLPP1 reduces Akt activation and inhibits melanoma cell proliferation in vitro, and retards melanoma growth in a xenograft model. In contrast, knockdown of PHLPP1 increases Akt activation, enhances melanoma cell and melanocyte proliferation, and results in anchorage-independent growth of melanocytes. Suppression of PHLPP1 involves blockade of binding of the transcription factor Sp1 to the PHLPP1 promoter. Collectively, these results suggest that suppression of PHLPP1 by DNA methylation contributes to melanoma development and progression.

DOI 10.1038/onc.2013.420
Citations Scopus - 9Web of Science - 6
Co-authors Lei Jin, Xu Zhang
2014 Tay KH, Luan Q, Croft A, Jiang CC, Jin L, Zhang XD, Tseng H-Y, 'Sustained IRE1 and ATF6 signaling is important for survival of melanoma cells undergoing ER stress', CELLULAR SIGNALLING, 26 287-294 (2014) [C1]
DOI 10.1016/j.cellsig.2013.11.008
Citations Scopus - 23Web of Science - 22
Co-authors Lei Jin, Xu Zhang
2014 Chi M, Chen J, Ye Y, Tseng H-Y, Lai F, Tay KH, et al., 'Adipocytes Contribute to Resistance of Human Melanoma Cells to Chemotherapy and Targeted Therapy', CURRENT MEDICINAL CHEMISTRY, 21 1255-1267 (2014) [C1]
Citations Scopus - 9Web of Science - 9
Co-authors Lei Jin, Xu Zhang
2014 Jiang CC, Croft A, Tseng HY, Guo ST, Jin L, Hersey P, Zhang XD, 'Repression of microRNA-768-3p by MEK/ERK signalling contributes to enhanced mRNA translation in human melanoma', Oncogene, 33 2577-2588 (2014) [C1]

Increased global protein synthesis and selective translation of mRNAs encoding proteins contributing to malignancy is common in cancer cells. This is often associated with elevate... [more]

Increased global protein synthesis and selective translation of mRNAs encoding proteins contributing to malignancy is common in cancer cells. This is often associated with elevated expression of eukaryotic translation initiation factor 4 (eIF4E), the rate-limiting factor of cap-dependent translation initiation. We report here that in human melanoma downregulation of miR-768-3p as a result of activation of the mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway has an important role in the upregulation of eIF4E and enhancement in protein synthesis. Melanoma cells displayed increased nascent protein production and elevated eIF4E expression, which was associated with the downregulation of miR-768-3p that was predicted to target the 3'-untranslated region of the eIF4E mRNA. Overexpression of miR-768-3p led to the downregulation of the endogenous eIF4E protein, reduction in nascent protein synthesis and inhibition of cell survival and proliferation. These effects were efficiently reversed when eIF4E was co-overexpressed in melanoma cells. On the other hand, introduction of anti-miR-768-3p into melanocytes upregulated endogenous eIF4E protein expression and increased global protein synthesis. Downregulation of miR-768-3p appeared to be mediated by activation of the MEK/ERK pathway, in that treatment of BRAF V600E melanoma cells with the mutant BRAF inhibitor PLX4720 or exposure of either BRAF V600E or wild-type BRAF melanoma cells to the MEK inhibitor U0126 resulted in the upregulation of miR-768-3p and inhibition of nascent protein synthesis. This inhibition was partially blocked in cells cointroduced with anti-miR-768-3p. Significantly, miR-768-3p was similarly downregulated, which was inversely associated with the expression levels of eIF4E in fresh melanoma isolates. Taken together, these results identify downregulation of miR-768-3p and subsequent upregulation of eIF4E as an important mechanism in addition to phosphorylation of eIF4E responsible for MEK/ERK-mediated enhancement of protein synthesis in melanoma. © 2014 Macmillan Publishers Limited.

DOI 10.1038/onc.2013.237
Citations Scopus - 15Web of Science - 12
Co-authors Lei Jin, Xu Zhang
2014 Liu Z, Zhang Y-Y, Zhang Q-W, Zhao S-R, Wu C-Z, Cheng X, et al., '3-Bromopyruvate induces apoptosis in breast cancer cells by downregulating Mcl-1 through the PI3K/Akt signaling pathway', ANTI-CANCER DRUGS, 25 447-455 (2014) [C1]
DOI 10.1097/CAD.0000000000000081
Citations Scopus - 20Web of Science - 20
2014 Zhang P, Liu H, Xia F, Zhang QW, Zhang YY, Zhao Q, et al., 'Epithelial-mesenchymal transition is necessary for acquired resistance to cisplatin and increases the metastatic potential of nasopharyngeal carcinoma cells', INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 33 151-159 (2014) [C1]
DOI 10.3892/ijmm.2013.1538
Citations Scopus - 18Web of Science - 18
2014 Sun XJ, Zhang P, Li HH, Jiang ZW, Jiang CC, Liu H, 'Cisplatin combined with metformin inhibits migration and invasion of human nasopharyngeal carcinoma cells by regulating E-cadherin and MMP-9', Asian Pacific Journal of Cancer Prevention, 15 4019-4023 (2014) [C1]

Metformin has been shown to be useful in reducing insulin resistance by restoring sensitivity. Recent evidence suggests that metformin might also possess anti-tumour activity. Thi... [more]

Metformin has been shown to be useful in reducing insulin resistance by restoring sensitivity. Recent evidence suggests that metformin might also possess anti-tumour activity. This study aimed to investigate the effects of cisplatin combined with metformin on the proliferation, invasion and migration of HNE1/DDP human nasopharyngeal carcinoma (NPC) cells, and to provide a new target for treating metastasis. The MTT assay was used to assess viability of HNE1/DDP cells after exposure to different concentrations of 2, 5-diaminopyrimidine-4, 6-diol (DDP; 2, 4, 8, 16, and 32 µmol·L -1 ), metformin (5, 10, 15, 20, and 25 µmol·L -1 ), and 4 µmol·L -1 of DDP combined with metformin. Wound healing and transwell migration assays were performed to assess cell migration and invasion, and expression of E-cadherin and MMP-9 was detected using Western blotting. MTT assay results showed that DDP could inhibit the proliferation of HNE1/DDP cells in a time- and concentration-dependent manner, with an IC50 of 32.0 µmol·L -1 at 24 h (P < 0.05), whereas low concentrations of DDP had almost no inhibitory effects on cell invasion and migration. DDP combined with metformin significantly inhibited cell invasion and migration. In addition, genes related to migration and invasion, such as those of E-cadherin and MMP-9, showed differential expression in the NPC cell line HNE1/DDP. In the present study, with an increasing concentration of metformin, the expression of MMP-9 was downregulated whereas that of E-cadherin was significantly upregulated. Taken together, our results show that cisplatin combined with metformin has effects on proliferation, invasion, and migration of human NPC cells.

DOI 10.7314/APJCP.2014.15.9.4019
Citations Scopus - 13Web of Science - 9
2013 Li Y, Liu H, Huang Y-Y, Pu L-J, Zhang X-D, Jiang Z-W, Jiang C-C, '[Effects of cisplatin combined with heparanase inhibitor on proliferation and invasion of human nasopharyngeal carcinoma cells].', Yao Xue Xue Bao, 48 609-614 (2013)
Citations Scopus - 1
Co-authors Xu Zhang
2013 Wroblewski D, Jiang CC, Croft A, Farrelly ML, Zhang XD, Hersey P, 'OBATOCLAX and ABT-737 induce ER stress responses in human melanoma cells that limit induction of apoptosis.', PLoS One, 8 e84073 (2013) [C1]
DOI 10.1371/journal.pone.0084073
Citations Scopus - 15Web of Science - 13
Co-authors Xu Zhang
2013 Zhang QW, Zhang YY, Zhao ZH, Zhang P, Jiang CC, Liu H, Jiang ZW, 'Influence of hydroxychloroquine on the proliferation and apoptosis of breast cancer cell MDA-MB-435', Chinese Pharmacological Bulletin, 29 1549-1553 (2013)

Aim: To observe the influence of hydroxychloroquine (HCQ) on the proliferation and apoptosis of breast cancer cell MDA-MB-435. Methods: The effect of HCQ on the proliferation of M... [more]

Aim: To observe the influence of hydroxychloroquine (HCQ) on the proliferation and apoptosis of breast cancer cell MDA-MB-435. Methods: The effect of HCQ on the proliferation of MDA-MB-435 cell was evaluated by MTT assay and clone formation assay; morphological changes of MDA-MB-435 cell after HCQ treatment was observed by inverted microscope; Hoechst 33258 staining was used to assess the changes in HCQ-induced apoptosis of MDA-MB-435 cell; PI staining was used to analyze the apoptosis of the cell exposed to HCQ; JC-1 was used to detect the changes of mitochondrial membrane potential of MDA-MB-435 cell. Results: Incubation with HCQ for 24 h, 48 h and 72 h resulted in a significant inhibition of MDA-MB-435 cell proliferation; HCQ treatment at different concentrations caused MDA-MB-435 cell turning round and shrinkage gradually, density of cell turning smaller gradually and losing the normal cell morphology; HCQ treatment also inhibited cell colony formation; Hoechst 33258 staining showed HCQ could induce apoptosis of MDA-MB-435 cell; exposure to 20, 40, 60 µmol · L -1 HCQ for 24 h caused a percentage of late apoptotic cells of 7.1%, 15.9%, 35.3% (P < 0.05); HCQ treatment at different concentrations also turned JC-1 from red to green (P < 0.05). Conclusion: HCQ can significantly inhibit the proliferation of MDA-MB-435 cell and induce apoptosis.

DOI 10.3969/j.issn.1001-1978.2013.11.018
Citations Scopus - 1
2013 Pu L, Huang Y, Li Y, Xu J, Jiang C, Liu H, Jiang Z, '[Small interfering RNA-mediated glucose-regulated protein 78 knockdown enhances chemosensitivity of breast cancer cells to cisplatin].', Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 33 44-47 (2013)

To investigate the effect of small interfering RNA-mediated glucose-regulated protein 78 (GRP78) knockdown on the chemosensitivity of breast cancer cells to cisplatin. Human breas... [more]

To investigate the effect of small interfering RNA-mediated glucose-regulated protein 78 (GRP78) knockdown on the chemosensitivity of breast cancer cells to cisplatin. Human breast cancer cell line MDA-MB-231 was exposed to different doses of cisplatin (0, 1, 2, 4, 8, and 16 µmol/L), and the changes in cell viability were detected using MTT assay. PI/Annexin V staining was used to observe the apoptosis of the cells in response to transfection with a small interfering RNA targeting GRP78 (pSH1Si-GRP78). Western blotting was employed to detect GRP78 expression in pSH1Si- GRP78-transfected cells after exposure to 8 µmol/L cisplatin for 24, 48 and 72 h. Exposure of the cells to 8 µmol/L cisplatin for 24, 48 and 72 h resulted in a cell survival rate of 83.13%, 54.22% and 35.79%, respectively, but the cell apoptosis rate was only 10.8% at 24 h. Transfection of MDA-MB-231 cells with pSH1Si-GRP78 caused a cell apoptosis rate of 24.6%, which increased to 48.9% in cells with both pSH1Si-GRP78 transfection and cisplatin exposure. Cisplatin exposure caused an initial up-regulation followed then by a down-regulation of GRP78 expression in MDA-MB-231 cells, while pSH1Si-GRP78 transfection produced an obvious down-regulation of GRP78 expression. Inhibition of GRP78 expression increases the apoptosis and enhance cisplatin chemosensitivity of breast cancer cells in vitro, suggesting the value of GRP78 as a potential therapeutic target in the clinical treatment of breast cancer.

Citations Scopus - 1
2013 Pu LJ, Liu H, Yang L, Huang YY, Xu JC, Zhang XD, et al., 'Knockdown GRP78 reverses resistance of human nasopharyngeal carcinoma to cisplatin-based chemotherapy and radiotherapy.', Asian Pac J Cancer Prev., 1003-1007 (2013)
2013 Tseng HY, Lai F, Jiang C, Kefford R, Long GV, Rizos H, Zhang XD, 'Inhibition of oncogenic BRAF triggers immunogenic cell death of human melanoma cells.', Journal Der Deutschen Dermatologieschen Gesellschaft, 257-259 (2013)
2013 Jin L, Dong L, Tseng HY, Wang CY, Wilmott JS, Yosufi B, et al., 'PHLPP1 deactivates Akt and has a tumor suppressive role in human melanoma.', Journal Der Deutschen Dermatologieschen Gesellschaft., 18-19 (2013)
2013 Xu J, Huang Y, Li Y, Pu L, Xia F, Jiang C, et al., '[Glycosylation inhibitor 2-deoxy-D-glucose sensitizes oral cancer cells to TRAIL-induced apoptosis].', Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 33 524-527 (2013)

To investigate the effect of 2-deoxy-D-glucose (2-DG) in enhancing the sensitivity of oral cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced ... [more]

To investigate the effect of 2-deoxy-D-glucose (2-DG) in enhancing the sensitivity of oral cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. The oral cancer cell line KB was incubated in the presence of different concentrations (0, 0.625, 1.25, 2.5, 5, and 10 mmol/L) of 2-DG with or without TRAIL (200 ng/ml). The cell viability was measured using MTT assay and cell apoptosis was detected using flow cytometry with propidium iodide (PI) staining. KB cells treated with 5 mmol/L 2-DG with or without TRAIL for 0, 6, 16, or 24 h were examined with Western blotting for protein expressions of death receptor 5 (DR5) and caspase-3. Treatment of the cells with 5 mmol/L 2-DG for 24, 48 and 72 h resulted in a cell viability of 25.25%, 69.06%, and 59.19%, respectively. Combined treatment with 5 mmol/L 2-DG with TRAIL for 24 significantly enhanced the cell apoptotic rate (72.5%) as compared to the rate induced by TRAIL alone (45.3%) and by 2-DG (15.9%) alone. 2-DG treatment markedly up-regulated DR5 and caspase-3 expression and enhanced the inhibitory effect of TRAIL on cell colony formation. 2-DG sensitizes oral cancer cells to TRAIL- induced apoptosis by up-regulating DR5 and caspase-3 expressions.

Citations Scopus - 1
2013 Pu L, Huang Y, Li Y, Xu J, Jiang C, Liu H, Jiang Z, 'Inhibition of GRP78 sensitizes breast cancer cells to Cisplatin', Nan Fang Yi Ke Da Xue Xue Bao, 44-47 (2013)
2013 Huang YY, Liu H, Li Y, Pu LJ, Jiang CC, Xu JC, Jiang ZW, 'Down-regulation of RIP1 by 2-deoxy-D-glucose sensitizes breast cancer cells to TRAIL-induced apoptosis', European Journal of Pharmacology, 705 26-34 (2013) [C1]
DOI 10.1016/j.ejphar.2013.02.005
Citations Scopus - 5Web of Science - 5
2013 Zhao SR, Duan HF, Zhang P, Liu H, Jiang C, Jiang ZW, '2-DG enhances TRAIL-induced apoptosis of leukemia HL-60 cells', Zhongguo Shi Yan Xue Ye Xue Za Zhi, 351-355 (2013)
2013 Xu J, Huang Y, Li Y, Pu L, Xia F, Jiang C, et al., '[Small interfering RNA-mediated RIP1 knockdown enhances L-OHP sensitivity of human oral squamous carcinoma cells].', Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 33 1004-1007 (2013)

To investigate the effect of small interfering RNA-mediated receptor-interacting protein kinase 1 (RIP1) knockdown on the sensitivity of human oral squamous carcinoma cells to to ... [more]

To investigate the effect of small interfering RNA-mediated receptor-interacting protein kinase 1 (RIP1) knockdown on the sensitivity of human oral squamous carcinoma cells to to oxaliplatin (L-OHP)-induced apoptosis and explore a new target for clinical treatment of oral squamous carcinoma. The viability of human oral squamous carcinoma cell line KB exposed to different concentrations (0, 0.25, 0.5, 1, 2, 4 µmol/L) of L-OHP were detected by MTT assay. PI/Annexin V staining was used to observe cell apoptosis in naive KB cells, cell and transfected with pSH1Si-RIP1 or with the empty plasmid. Western blotting was used to detect RIP1 expression in KB cells exposed to L-OHP and in cells transfected with pSH1Si-RIP1. Exposure to L-OHP (1µmol/L) for 24, 48, 72 h resulted in KB cell survival rates of 67.66%, 55.17%, and 41.34%, respectively, but the cell apoptosis rate was only 9.6% following a 24-h exposure. KB cells transfected with pSH1Si-RIP1 showed an apoptotic rate of 9.4%, which increased to 29.1% following L-OHP exposure. RIP1 expression was first up-regulated and then down-regulated in KB cells treated with L-OHP, and was significantly reduced after cell transfection with pSH1Si-RIP1. Suppression of RIP1 expression increases the apoptotic rate of human oral squamous carcinoma cells, suggesting the potential of RIP1 as a new candidate target for clinical treatment of oral squamous carcinoma.

Citations Scopus - 2
2013 Zhang Y, Liu Z, Zhang Q, Chao Z, Zhang P, Xia F, et al., '[Effect of 3-bromopyruvate on mitochondrial membrane potential and apoptosis of human breast carcinoma SK-BR-3 cells].', Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 33 1304-1307 (2013)

To study the effect of glycolysis inhibitor 3-bromopyruvate (3-BrPA) in inducing apoptosis of human breast carcinoma cells SK-BR-3 and the possible mechanism. MTT assay was used t... [more]

To study the effect of glycolysis inhibitor 3-bromopyruvate (3-BrPA) in inducing apoptosis of human breast carcinoma cells SK-BR-3 and the possible mechanism. MTT assay was used to detect the growth inhibition induced by 3-BrPA in breast cancer cells SK-BR-3. The apoptotic cells were detected by flow cytometry with propidium iodide (PI). ATP levels in the cells were detected by ATP assay kit, and DHE fluorescent probe technique was used to determine superoxide anion levels; the mitochondrial membrane potential was assessed using JC-1 staining assay. MTT assay showed that the proliferation of SK-BR-3 cells was inhibited by 3-BrPA in a time- and concentration-dependent manner. Exposure to 80, 160, and 320 µmol·L(-1) 3-BrPA for 24 h resulted in cell apoptosis rates of 6.7%, 22.3%, and 79.6%, respectively, and the intracellular ATP levels of SK-BR-3 cells treated with 80, 160, 320 µmol·L(-1) 3-BrPA for 5 h were 87.7%, 60.6%, and 23.7% of the control levels. 3-BrPA at 160 µmol·L(-1) increased reactive oxygen levels and lowered mitochondrial membrane potential of SK-BR-3 cells. 3-BrPA can inhibit cell proliferation, reduce the mitochondrial membrane potential and induce apoptosis in SK-BR-3 cells, the mechanism of which may involve a reduced ATP level by inhibiting glycolysis and increasing the reactive oxygen level in the cells.

2013 Guo ST, Jiang CC, Wang GP, Li YP, Wang CY, Guo XY, et al., 'MicroRNA-497 targets insulin-like growth factor 1 receptor and has a tumour suppressive role in human colorectal cancer', ONCOGENE, 32 1910-1920 (2013) [C1]
DOI 10.1038/onc.2012.214
Citations Scopus - 123Web of Science - 108
Co-authors Xu Zhang, Lei Jin, Rick Thorne
2013 Li Y, Liu H, Huang YY, Pu LJ, Zhang XD, Jiang CC, Jiang ZW, 'Suppression of endoplasmic reticulum stress-induced invasion and migration of breast cancer cells through the downregulation of heparanase', INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 31 1234-1242 (2013) [C1]
DOI 10.3892/ijmm.2013.1292
Citations Scopus - 21Web of Science - 19
Co-authors Xu Zhang
2013 Sun X-J, Liu H, Zhang P, Zhang X-D, Jiang Z-W, Jiang C-C, 'miR-10b Promotes Migration and Invasion in Nasopharyngeal Carcinoma Cells', ASIAN PACIFIC JOURNAL OF CANCER PREVENTION, 14 5533-5537 (2013) [C1]
DOI 10.7314/APJCP.2013.14.9.5533
Citations Scopus - 29Web of Science - 26
Co-authors Xu Zhang
2013 Song L, Liu H, Ma L, Zhang X, Jiang Z, Jiang C, 'Inhibition of autophagy by 3-MA enhances endoplasmic reticulum stress-induced apoptosis in human nasopharyngeal carcinoma cells', ONCOLOGY LETTERS, 6 1031-1038 (2013) [C1]
DOI 10.3892/ol.2013.1498
Citations Scopus - 14Web of Science - 14
Co-authors Xu Zhang
2013 Ye Y, Jin L, Wilmott JS, Hu WL, Yosufi B, Thorne RF, et al., 'PI(4,5)P2 5-phosphatase A regulates PI3K/Akt signalling and has a tumour suppressive role in human melanoma', NATURE COMMUNICATIONS, 4 (2013) [C1]
DOI 10.1038/ncomms2489
Citations Scopus - 39Web of Science - 38
Co-authors Lei Jin, Xu Zhang, Rick Thorne
2013 Lai F, Guo ST, Jin L, Jiang CC, Wang CY, Croft A, et al., 'Cotargeting histone deacetylases and oncogenic BRAF synergistically kills human melanoma cells by necrosis independently of RIPK1 and RIPK3', CELL DEATH & DISEASE, 4 (2013) [C1]
DOI 10.1038/cddis.2013.192
Citations Scopus - 20Web of Science - 20
Co-authors Lei Jin, Xu Zhang
2013 Hu W, Jin L, Jiang CC, Long GV, Scolyer RA, Wu Q, et al., 'AEBP1 upregulation confers acquired resistance to BRAF (V600E) inhibition in melanoma.', Cell Death and Disease, 4 e914 (2013) [C1]
DOI 10.1038/cddis.2013.441
Citations Scopus - 13Web of Science - 13
Co-authors Lei Jin, Xu Zhang
2013 Xu JC, Li Y, Liu H, Huang YY, Pu LJ, Xia F, et al., 'Invasion and migration effects of heparanase inhibitor OGT2115 on oral cancer cell', Chinese Pharmacological Bulletin, 29 525-530 (2013)

Aim: To investigate the inhibitory effect of heparanase inhibitor OGT2115 on the invasion and migration in KB cells, in order to provide a new target points for the treatment of c... [more]

Aim: To investigate the inhibitory effect of heparanase inhibitor OGT2115 on the invasion and migration in KB cells, in order to provide a new target points for the treatment of cancer metastasis. Methods: MTT assay was used to detect the cell viability by different concentrations of OGT2115 (0.4, 0.8, 1.6, 3.2, 6.4 µmol·L -1 ) and OGT2115 (0.4 µmol·L -1 ) combine with ADM(2 µmol·L -1 ) in KB. Transwell assay was applied to detect the invasion and migration by OGT2115 and ADM. Wound healing assay was employed to observe cell migration, and heparanase activity was detected by ELISA. Results: MTT results showed that OGT2115 could inhibit the proliferation of KB; IC 50 was 8.59 µmol·L -1 ; the inhibitory activity increased with the role of time and concentration(P < 0.05). OGT2115 could inhibit the invasion and migration of KB; using OGT2115(0.4 µmol·L -1 ) significantly enhanced anti-invasion and anti- proliferation of ADM (P < 0.05). Conclusion: OGT2115 can inhibit the invasion and migration of KB, and OGT2115 enhances anti-invasion and anti- migration of ADM, which is closely related to heparanase.

DOI 10.3969/j.issn.1001-1978.2013.04.018
Citations Scopus - 1
2013 Huang YY, Liu H, Li Y, Pu LJ, Zhang XD, Jiang CC, Jiang ZW, '2-DG sensitizes nasopharyngeal carcinoma cells to TRAIL induced apoptosis', Chinese Pharmacological Bulletin, 29 1119-1124 (2013)

Aim: To determine whether 2-DG (2-deoxy-D-glucose) can synergize with tumors necrosis factor-related apotosis-inducing ligand (TRAIL) which is used in nasopharyngeal carcinoma tre... [more]

Aim: To determine whether 2-DG (2-deoxy-D-glucose) can synergize with tumors necrosis factor-related apotosis-inducing ligand (TRAIL) which is used in nasopharyngeal carcinoma treatment and wish to find new targets for human nasopharyngeal carcinoma chemotherapy. Methods: Nasopharyngeal carcinoma cells CNE-2 were incubated with varying concentrations of 2-DG (0, 0.625, 1.25, 2.5, 5, 10 mmol·L -1 ) with or without TRAIL (200 µg·L -1 ). Cell viability was measured by the MTT (3-(4, 5-dimethylthiazol-2-yl)-2-5 diphenyltetrazolium bromide) assay. Then propidium iodide (PI) staining was used to measure apoptotic cells in Flow Cytometry (FCM). CNE-2 cells were treated with 2-DG (5 mmol·L -1 ) (with or without TRAIL) for different time points (0, 6, 16, 24 h). Western blot was used to measure the protein expression of glucose-regulated protein 78 (GRP-78) and Caspase-3. Results: Combining 2-DG with TRAIL resulted in enhanced cell death compared with the individual use of each agent, 2-DG induced apoptosis cells hardly reached 10% and 2-DG markedly up-regulated GRP-78 and Caspase-3 expression. With the combination of 2-DG and TRAIL, the apoptotic rate of CNE-2 cells reached 78.9%. Conclusion: These results indicate that 2-DG sensitizes nasopharyngeal carcinoma cells to TRAIL induced apoptosis by up-regulation of GRP-78 and Caspase-3.

DOI 10.3969/j.issn.1001-1978.2013.08.018
Citations Scopus - 1
Co-authors Xu Zhang
2012 Song L, Ma L, Zhang X, Jiang Z, Liu H, Jiang C, '[Effect of tunicamycin combined with cisplatin on proliferation and apoptosis of human nasopharyngeal carcinoma cells in vitro].', Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 32 766-771 (2012)

To study the effects of tunicamycin (a glycosylation inhibitor) combined with cisplatin on the proliferation and apoptosis of human nasopharyngeal carcinoma cells and explore the ... [more]

To study the effects of tunicamycin (a glycosylation inhibitor) combined with cisplatin on the proliferation and apoptosis of human nasopharyngeal carcinoma cells and explore the molecular mechanism. Nasopharyngeal carcinoma CNE-1 and CNE-2 cells cultured in vitro were treated with different concentrations of tunicamycin with or without cisplatin. The inhibition of cell proliferation was examined using MTT assay and colony formation assay, and the cell apoptosis was analyzed using flow cytometry with propidium iodide staining. The expressions of Bax, Bcl-2, and GRP78 in cells treated with 3 µmol/L tunicamycin with or without 6.00 µmol/L cisplatin were measured with Western blotting. Treatment with tunicamycin or cisplatin obviously inhibited the proliferation of CNE-1 and CNE-2 cells. Treatment with 3 µmol/L tunicamycin for 24, 36 and 48 h resulted in a viability of 72.13%, 51.97%, and 37.56% in CNE-1 cells and 85.61%, 56.95%, and 43.66% in CNE-2 cells, respectively, and the combined treatment with 6 µmol/L cisplatin lowered the cell viability to 67.97%, 47.76%, and 34.68% in CNE-1 cells and 56.89%, 37.05%, and 29.30% in CNE-2 cells, respectively. Tunicamycin at 0.3 µmol/L combined with 0.6 µmol/L cisplatin showed an obviously enhanced inhibitory effect on colony formation of CNE-1 and CNE-2 cells. Tunicamycin treatment (3 µmol/L) of CNE-1 and CNE-2 cells for 48 h induced an apoptosis rate of only 8.89% and 8.67%, but when combined with 6 µmol/L cisplatin, the cell apoptosis rate increased to 37.02% and 32.25%, significantly higher than that in cells with cisplatin treatment alone (7.25% and 6.36%, respectively). Compared with tunicamycin and cisplatin alone, the combined treatment significantly increased Bax expression and decreased Bcl-2 expression in the cells; tunicamycin up-regulated the expression of GRP-78 and enhanced the activity of caspase-3. Tunicamycin can inhibit the proliferation of CNE-1 and CNE-2 cells and enhance cisplatin-induced cell death, the mechanism of which may involve excessive endoplasmic reticulum stress response and increased activity of caspase-3.

Citations Scopus - 2
2012 Tseng HY, Chen L, Ye Y, Tay KH, Jiang CC, Guo ST, et al., 'The melanoma-associated antigen MAGE-D2 suppresses TRAIL receptor 2 and protects against TRAIL-induced apoptosis in human melanoma cells', Carcinogenesis, 33 1871-1881 (2012) [C1]
Citations Scopus - 13Web of Science - 12
Co-authors Xu Zhang, Lei Jin
2012 Lai FS, Jiang CC, Farrelly ML, Zhang XD, Hersey P, 'Evidence for upregulation of Bim and the splicing factor SRp55 in melanoma cells from patients treated with selective BRAF inhibitors', Melanoma Research, 22 244-251 (2012) [C1]
Citations Scopus - 16Web of Science - 15
Co-authors Xu Zhang
2012 Tay KH, Jin L, Tseng HY, Jiang CC, Ye Y, Thorne RF, et al., 'Suppression of PP2A is critical for protection of melanoma cells upon endoplasmic reticulum stress', Cell Death and Disease, 3 (2012) [C1]
DOI 10.1038/cddis.2012.79
Citations Scopus - 21Web of Science - 20
Co-authors Nikki Verrills, Rick Thorne, Xu Zhang, Lei Jin
2012 Zhang P, Zhao S, Song L, Pu L, Jiang Z, Liu H, Jiang C, '[Effect of low-molecular-weight heparin combined with paclitaxel on the invasiveness and migration of nasopharyngeal carcinoma cells in vitro].', Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 32 1529-1535 (2012)

To investigate the effect of low-molecular-weight heparin (LMWH) combined with paclitaxel (PTX) on the invasiveness and migration of nasopharyngeal carcinoma cells and explore the... [more]

To investigate the effect of low-molecular-weight heparin (LMWH) combined with paclitaxel (PTX) on the invasiveness and migration of nasopharyngeal carcinoma cells and explore the molecular mechanisms. MTT assay was used to detect the growth inhibition induced by LMWH and PTX in CNE1 and CNE2 cells. Wound healing assay and Transwell migration assay were employed to assess the effects of the drugs on the cell migration, and Transwell invasion assay was used to evaluate the cell invasiveness. The cellular expression of matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) were analyzed by Western blotting. ELISA was used to determine the expression of heparanase (HPA) in the culture medium of the cells. MTT assay showed an obvious suppression of CNE1 and CNE2 cell proliferation in response to LMWH and PTX treatments. Treatment with 200 U·ml LMWH combined with 0.1 µmol·L PTX for 24 h resulted in the inhibition rates of migration of 66.70% and 70.53% in CNE1 and CNE2 cells, respectively significantly higher than the rates in cells with PTX treatment alone. The combined treatment with LMWH and PTX for 24 h also caused a significantly higher inhibition rate of cell invasion than LMWH and PTX alone. LMWH enhanced the down-regulation of MMP-9 and HPA induced by PTX. LMWH can enhance the inhibitory effect of PTX on the migration and invasion of nasopharyngeal carcinoma cells, the mechanism of which may involve the down-regulation of MMP-9 and HPA expressions.

2011 Jiang CC, Lai F, Thorne RF, Yang F, Liu H, Hersey P, Zhang XD, 'MEK-independent survival of B-RAFV600E melanoma cells selected for resistance to apoptosis induced by the RAF inhibitor PLX4720', Clinical Cancer Research, 17 721-730 (2011) [C1]
DOI 10.1158/1078-0432.CCR-10-2225
Citations Scopus - 70Web of Science - 66
Co-authors Rick Thorne, Xu Zhang
2011 Liu H, Jiang CC, Cheng X, Fang L, Chen C, Zhang XD, Jiang ZW, 'Effects of resveratrol on proliferation and apoptosis in human melanoma cells', Chinese Pharmacological Bulletin, 27 998-1002 (2011)

Aim: To investigate the effect of resveratrol (Res) on the proliferation and apoptosis in human melanoma cells. Methods: Mel-RM and MM200 cells were treated with different concent... [more]

Aim: To investigate the effect of resveratrol (Res) on the proliferation and apoptosis in human melanoma cells. Methods: Mel-RM and MM200 cells were treated with different concentrations of Res. Cell viability was measured using the MTT assay. Apoptosis induced by Res was examined using the propidium iodide (PI) staining in flow cytometry. Mitochondrial membrane potential (¿¿m) in Mel-RM and MM200 cells was detected by JC-1 staining. Activation of Caspase-3 was detected by special kit. Results: Cell viability was inhibited by Res with the increasing concentration. 80, 160 µmol·L -1 Res could induces obvious apoptosis in melanoma Mel-RM and MM200 cells. JC-1 staining results showed that Res could decrease the mitochondrial membrane potential in Mel-RM and MM200 cells. It also induced the activation of Caspases-3. Conclusions: Res can inhibit the proliferation and induce apoptosis in melanoma Me1-RM and MM200 cells. The effect might be associated with the reduction of ¿¿m and the activation of Caspase-3.

DOI 10.3969/j.issn.1001-1978.2011.07.025
Citations Scopus - 3
Co-authors Xu Zhang
2011 Jin L, Hu WL, Jiang CC, Wang JX, Han CC, Chu P, et al., 'MicroRNA-149*, a p53-responsive microRNA, functions as an oncogenic regulator in human melanoma', Proceedings of the National Academy of Sciences, 108 15840-15845 (2011) [C1]
DOI 10.1073/pnas.1019312108
Citations Scopus - 98Web of Science - 94
Co-authors Lei Jin, Xu Zhang, Rick Thorne
2011 Dong L, Jiang CC, Thorne RF, Croft A, Yang F, Liu H, et al., 'Ets-1 mediates upregulation of Mcl-1 downstream of XBP-1 in human melanoma cells upon ER stress', Oncogene, 30 3716-3726 (2011) [C1]
DOI 10.1038/onc.2011.87
Citations Scopus - 36Web of Science - 35
Co-authors Xu Zhang, Rick Thorne
2010 Jiang CC, Lai F, Tay KH, Croft A, Rizos H, Becker TM, et al., 'Apoptosis of human melanoma cells induced by inhibition of B-RAF(V600E) involves preferential splicing of bim(S)', Cell Death & Disease, 1 e69 (2010) [C1]
DOI 10.1038/cddis.2010.48
Citations Scopus - 66Web of Science - 61
Co-authors Rick Thorne, Xu Zhang
2010 Tseng HY, Jiang C, Croft A, Tay KH, Throng RF, Yang F, et al., 'Contrasting Effects of Nutlin-3 on TRAIL- and Docetaxel-Induced Apoptosis Due to Upregulation of TRAIL-R2 and Mcl-1 in Human Melanoma Cells', Mol Cancer Ther, 3363-3374 (2010)
2010 Yang F, Tay KH, Dong L, Thorne RF, Jiang CC, Yang E, et al., 'Cystatin B inhibition of TRAIL-induced apoptosis is associated with the protection of FLIPL from degradation by the E3 ligase itch in human melanoma cells', Cell Death and Differentiation, 17 1354-1367 (2010) [C1]
DOI 10.1038/cdd.2010.29
Citations Scopus - 34Web of Science - 31
Co-authors Rick Thorne, Xu Zhang
2010 Mao ZG, Jiang CC, Thorne RF, Hersey P, Zhang XD, 'TRAIL-induced apoptosis of human melanoma cells involves activation of caspase-4', Apoptosis, 15 1211-1222 (2010) [C1]
DOI 10.1007/s10495-010-0513-9
Citations Scopus - 18Web of Science - 16
Co-authors Xu Zhang, Rick Thorne
2009 Liu H, Jiang CC, Lavis CJ, Croft A, Dong L, Tseng H-Y, et al., '2-Deoxy-D-glucose enhances TRAIL-induced apoptosis in human melanoma cells through XBP-1-mediated up-regulation of TRAIL-R2', Molecular Cancer, 8 Article no. 122 (2009) [C1]
DOI 10.1186/1476-4598-8-122
Citations Scopus - 41Web of Science - 33
Co-authors Xu Zhang
2009 Jiang CC, Yang F, Thorne RF, Zhu BK, Hersey P, Zhang XD, 'Human melanoma cells under endoplasmic reticulum stress acquire resistance to microtubule-targeting drugs through XBP-1-mediated activation of Akt', Neoplasia, 11 436-447 (2009) [C1]
DOI 10.1593/neo.09208
Citations Scopus - 38Web of Science - 33
Co-authors Xu Zhang, Rick Thorne
2009 Jiang CC, Wroblewski D, Yang F, Hersey P, Zhang XD, 'Human melanoma cells under endoplasmic reticulum stress are more susceptible to apoptosis induced by the BH3 mimetic obatoclax', Neoplasia, 11 945-955 (2009) [C1]
DOI 10.1593/neo.09692
Citations Scopus - 35Web of Science - 31
Co-authors Xu Zhang
2009 Jiang CC, Mao ZG, Kiejda KA, Hersey P, Zhang XD, 'Glucose-regulated protein 78 antagonizes cisplatin and adriamycin in human melanoma cells', Carcinogenesis, 30 197-204 (2009) [C1]
DOI 10.1093/carcin/bgn220
Citations Scopus - 60Web of Science - 58
Co-authors Xu Zhang, Kelly Kiejda
2008 Zhang XD, Jiang C, Kiejda KA, Lucas K, Wade M, Allen J, Hersey P, 'Up-regulation of Mcl-1 by the unfolded protein response is critical for survival of melanoma cells upon ER stress.', Pigment Cell Melanoma Res., 257-277 (2008)
2008 Chen LH, Jiang CC, Watts R, Thorne RF, Kiejda KA, Zhang XD, Hersey P, 'Inhibition of endoplasmic reticulum stress-induced apoptosis of melanoma cells by the ARC protein', Cancer Research, 68 834-842 (2008) [C1]
DOI 10.1158/0008-5472.can-07-5056
Citations Scopus - 32Web of Science - 28
Co-authors Rick Thorne, Kelly Kiejda, Xu Zhang
2008 Jiang CC, Lucas K, Kiejda KA, Wade M, Debock CE, Thorne RF, et al., 'Up-regulation of Mcl-1 is critical for survival of human melanoma cells upon endoplasmic reticulum stress', Cancer Research, 68 6708-6717 (2008) [C1]
DOI 10.1158/0008-5472.can-08-0349
Citations Scopus - 89Web of Science - 88
Co-authors Xu Zhang, Rick Thorne, Kelly Kiejda
2008 Zhu B-K, Wang P, Zhang XD, Jiang CC, Chen LH, Kiejda KA, et al., 'Activation of Jun N-terminal kinase is a mediator of vincristine-induced apoptosis of melanoma cells', Anti-Cancer Drugs, 19 189-200 (2008) [C1]
DOI 10.1097/CAD.0b013e3282f3138a
Citations Scopus - 25Web of Science - 25
Co-authors Kelly Kiejda, Xu Zhang
2007 Mhaidat NM, Zhang XD, Jiang CC, Hersey P, 'Docetaxel-induced apoptosis of human melanoma is mediated by activation of c-Jun NH2-terminal kinase and inhibited by the mitogen-activated protein kinase extracellular signal-regulated kinase 1/2 pathway', Clinical Cancer Research, 13 1308-1314 (2007) [C1]
DOI 10.1158/1078-0432.ccr-06-2216
Citations Scopus - 53Web of Science - 50
Co-authors Xu Zhang
2007 Yu FW, Jiang CC, Kiejda KA, Gillespie S, Zhang XD, Hersey P, 'Apoptosis induction in human melanoma cells by inhibition of MEK is caspase-independent and mediated by the Bcl-2 family members PUMA, Bim, and Mcl-1', Clinical Cancer Research, 13 4934-4942 (2007) [C1]
DOI 10.1158/1078-0432.CCR-07-0665
Citations Scopus - 120Web of Science - 123
Co-authors Kelly Kiejda, Xu Zhang
2007 Hersey P, Zhang XD, Jiang C, 'Endoplasmic stress (ER) in melanoma cells.', Arch Dermatol Res., 289-299 (2007)
2007 Jiang CC, Li HC, Gillespie S, Kiejda KA, Mhaidat N, Yu FW, et al., 'Tunicamycin sensitizes human melanoma cells to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by up-regulation of TRAIL-R2 via the unfolded protein response', Cancer Research, 67 5880-5888 (2007) [C1]
DOI 10.1158/0008-5472.CAN-07-0213
Citations Scopus - 82Web of Science - 81
Co-authors Xu Zhang, Kelly Kiejda, Rick Thorne
2007 Jiang CC, Li HC, Gillespie S, Yu FW, Kiejda KA, Zhang XD, Hersey P, 'Inhibition of MEK sensitizes human melanoma cells to endoplasmic reticulum stress-induced apoptosis', Cancer Research, 67 9750-9761 (2007) [C1]
DOI 10.1158/0008-5472.CAN-07-2047
Citations Scopus - 95Web of Science - 89
Co-authors Xu Zhang, Kelly Kiejda
2007 Chen LH, Jiang CC, Kiejda KA, Wang YF, Thorne RF, Zhang XD, Hersey P, 'Thapsigargin sensitizes human melanoma cells to TRAIL-induced apoptosis by up-regulation of TRAIL-R2 through the unfolded protein response', Carcinogenesis, 28 2328-2336 (2007) [C1]
DOI 10.1093/carcin/bgm173
Citations Scopus - 33Web of Science - 29
Co-authors Kelly Kiejda, Rick Thorne, Xu Zhang
Show 88 more journal articles

Conference (101 outputs)

Year Citation Altmetrics Link
2016 Jin L, Tabatabaee H, Yan XG, Wang JY, Zhang YY, Yari H, et al., 'A MICROFILAMENT PROTEIN AS A MASTER SWITCH AT THE INTERSECTION OF SURVIVAL SIGNALING PATHWAYS IN MELANOMA', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Xu Zhang
2016 Zhang YY, Wang JY, Wang CY, Guo ST, Yan XG, Farrelly M, et al., 'APOPTOSIS-REGULATING LONG NONCODING RNAS IN MELANOMA', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Citations Web of Science - 1
Co-authors Xu Zhang
2016 Wang YF, Liu F, Ji GY, Sherwin S, McFarlane J, Tseng H-Y, et al., 'IDENTIFICATION OF A NOVEL TRANSCRIPTION FACTOR COMPLEX IN CLASS I HDACS-MEDIATED UPREGULATION OF PD-L1 IN CANCER CELLS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Xu Zhang
2016 La T, Farrelly M, Wang JY, Wang CY, Yan XG, Zhang YY, et al., 'TOWARDS TARGETING QUIESCENT MELANOMA CELLS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Xu Zhang
2016 Lei F, Jin L, Yan XG, Liu F, Wang JY, Wang CY, et al., 'RIPK1 PROMOTES MELANOMA CELL SURVIVAL UPON MAPK INHIBITION', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Xu Zhang
2016 Liu F, Tseng CH-Y, Jin L, Zhang XD, Jiang CC, 'MAPK REGULATES CD47 EXPRESSION IN MELANOMA CELLS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Xu Zhang
2016 Wang CY, Guo ST, Wang JY, Yan XG, Farrelly M, Zhang YY, et al., 'REACTIVATION OF ERK AND AKT CONFERS RESISTANCE OF MUTANT BRAF COLON CANCER CELLS TO THE HSP90 INHIBITOR AUY922', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Xu Zhang
2016 Wang JY, Jin L, Yan XG, Sherwin S, Farrelly M, Zhang YY, et al., 'REACTIVE OXYGEN SPECIES DICTATE THE APOPTOTIC RESPONSE OF MELANOMA CELLS TO TH588', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Xu Zhang
2016 Yari H, Jin L, Wang JY, Wang CY, Liu F, Zhang YY, et al., 'AN ONCOGENIC LONG NONCODING RNA IN HUMAN COLON CANCER', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2016)
Co-authors Xu Zhang
2015 Jiang CC, Chi MN, Guo ST, Wilmott JS, Guo XY, Yan XG, et al., 'Inositol polyphosphate 4-phosphatase II activates PI3K/SGK3 signaling to promote proliferation of human melanoma cells', CANCER RESEARCH (2015) [E3]
DOI 10.1158/1538-7445.AM2015-4718
Co-authors Hubert Hondermarck, Xu Zhang, Lei Jin
2015 Jiang C, Chi MN, Zhang XD, 'MicroRNA regulation of INPP4B to promote melanoma cell proliferation through PI3K/SGK3.', 107th AACR Annual Meeting 2015,, Philadelphia, USA (2015) [O1]
2015 Jin L, Liu XY, Lai F, Yan XG, Jiang C, Guo ST, et al., 'Receptor-Interacting Protein Kinase 1 Functions as an oncogenic regulator in human melanoma', Cancer Research, Philadelphia, USA (2015) [E3]
Co-authors Lei Jin, Xu Zhang
2015 Wang CY, Jiang C, Zhang XD, 'Targeting MEK.ERK and PI3K/Akt to overcome resistance of human colon cancer to HSP90 inhibitor.', 27th Lorne Cancer Conference, Lorne, Australia (2015) [O1]
2015 Jin L, Liu XY, Yan XG, Jiang C, Guo ST, Wang CY, et al., 'Receptor-Interacting Protein Kinase 1 Functions as an oncogenic regulator in human melanoma.', 27th Lorne Cancer Conference, Lorne, Australia (2015) [O1]
2015 Guo ST, Chi M, Rang RH, Cuo XY, Wang CY, Zan LQ, et al., 'Inositol polyphosphate 4-phosphatase II promotes PI3K signaling and functions as an oncogenic regulator in human colon cancer', 27th Lorne Cancer Conference, Lorne, Australia (2015) [E3]
2015 Jiang C, Chi MN, Zhang XD, 'MicroRNA regulation of INPP4B to promote melanoma cell proliferation through PI3K/SGK3', 27th Lorne Cancer Conference, Lorne, Australia (2015) [E3]
2015 Wang JU, Wang CY, Jiang C, Tseng HY, Guo ST, Jin L, Zhang XD, 'Regulation of sensitivity of human melanoma cells to killing by the human Mut T homolog1 inhibitor.', 27th Lorne Cancer Conference, Lorne, Australia. (2015) [O1]
2015 Tseng HY, Luan Q, Jin L, Jiang C, Tay KH, Lai F, et al., 'Receptor-Interacting Protein Kinase 1 regulates survival of human melanoma cells upon endoplasmic reticulum stress through autophagy.', 27th Lorne Cancer Conference, Lorne, Australia (2015) [O1]
2015 Yan XG, Luan Q, Jin L, Jiang CC, Tay KH, Lai F, et al., 'Receptor-interacting protein kinase 1 regulates survival of human melanoma cells upon endoplasmic reticulum stress through autophagy', CANCER RESEARCH (2015) [E3]
DOI 10.1158/1538-7445.AM2015-1029
Co-authors Xu Zhang, Lei Jin
2015 Liu XY, Lai F, Yan XG, Jiang CC, Guo ST, Wang CY, et al., 'RIP1 kinase is an oncogenic driver in melanoma', INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE (2015) [E3]
Co-authors Xu Zhang, Lei Jin
2014 Jin L, Liu XY, Lai F, Yan XG, Jiang C, Guo ST, et al., 'Receptor-Interacting Protein Kinase 1 Functions as an oncogenic regulator in human melanoma.', Hunter Cancer Research Symposium, Newcastle, Australia (2014) [E3]
Co-authors Xu Zhang, Lei Jin
2014 Tseng HY, Luan Q, Jin L, Jiang C, Tay KH, Lai F, et al., 'Receptor-Interacting Protein Kinase 1 regulates survival of human melanoma cells upon endoplasmic reticulum stress through autophagy', Hunter Cancer Research Symposium, Newcastle, Australia (2014) [E3]
Co-authors Lei Jin, Xu Zhang
2014 Jiang C, Chi MN, Guo ST, Wilmott JS, Guo XG, Yan XG, et al., 'MicroRNA regulation of inositol polyphosphate 4-phosphatase II to modulate melanocytic cell proliferation through PI3K/SGK3 signaling', Hunter Cancer Research Symposium, Newcastle, Australia (2014) [E3]
Co-authors Xu Zhang
2014 Chi MN, Chen J, Ye Y, Tseng HY, Lai F, Tay KH, et al., 'Adipocytes contribute to resistance of human melanoma cells to chemotherapy and targeted therapy.', The Australian Society for Medical Research (ASMR) Satellite Scientific Meeting, Newcastle, Australia (2014) [E3]
Co-authors Xu Zhang, Lei Jin
2014 Wang CY, Jiang C, Chi MN, Croft A, Guo ST, Zhang XD, 'Reactivation of Akt and ERK protects against HSP90 inhibitors in human colon cancer cells.', The Australian Society for Medical Research (ASMR) Satellite Scientific Meeting., Newcastle, Australia (2014) [E3]
Co-authors Xu Zhang
2014 Lai F, Guo ST, Jin L, Jiang C, Wang CY, Croft A, et al., 'Cotargeting histone deacetylases and oncogenic BRAF synergistically kills melanoma cells by necrosis independently of RIPK1 and RIPK3.', The Australian Society for Medical Research (ASMR) Satellite Scientific Meeting., Newcastle, Australia (2014) [E3]
Co-authors Lei Jin, Xu Zhang
2014 Wang CY, Jiang CC, Guo ST, Croft A, Jin L, Tseng H-Y, et al., 'TARGETING MEK/ERK AND PI3K/AKT TO OVERCOME RESISTANCE OF HUMAN COLON CANCER TO HSP90 INHIBITORS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Xu Zhang, Lei Jin
2014 Croft A, Tay KH, Philipsz S, Jiang CC, Lai F, Tseng H-Y, et al., 'ONCOGENIC ACTIVATION OF MEK/ERK PRIMES MELANOMA CELLS FOR ADAPTATION TO ENDOPLASMIC RETICULUM STRESS', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Xu Zhang, Lei Jin
2014 Guo ST, Chi MN, Yang RH, Guo XY, Wang CY, Zan LQ, et al., 'INOSITOL POLYPHOSPHATE 4-PHOSPHATASE II PROMOTES PI3K SIGNALING AND FUNCTIONS AS AN ONCOGENIC REGULATOR IN HUMAN COLON CANCER', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Rick Thorne, Stephen Ackland, Xu Zhang, Lei Jin, Rodney Scott
2014 Wang JY, Wang CY, Jiang CC, Tseng H-Y, Guo ST, Jin L, Zhang XD, 'REGULATION OF SENSITIVITY OF HUMAN MELANOMA CELLS TO KILLING BY THE HUMAN MUT T HOMOLOG1 INHIBITOR', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2014) [E3]
Co-authors Xu Zhang, Lei Jin
2013 Guo ST, Lal F, Jiang CC, Wang CY, Farrelly M, Tseng H-Y, et al., 'Co-targeting histone deacetylases and oncogenic BRAF synergistically kills human melanoma cell by caspase-independent cell death.', CANCER RESEARCH, Washington, DC (2013) [E3]
DOI 10.1158/1538-7445.AM2013-2028
Co-authors Xu Zhang
2013 Jiang C, Zhang XD, 'Inhibition of oncogenic BRAF triggers immunogenic necrosis of human melanoma cells.', 8th World Congress of Melanoma, Hamburg, Germany (2013)
2013 Zhang XD, Jiang C, 'PHLPP1 deactivates Akt and has a tumor suppressive role in human melanoma.', 8th World Congress of Melanoma, Hamburg, Germany (2013)
2013 Croft A, Tay KH, Philipse S, Jiang C, Lai F, Tseng HY, Zhang XD, 'Oncogenic activation of MEK/ERK primes melanoma cells for adaptation to endoplasmic reticulum stress', HCRA Translational Cancer Research Conference, Newcastle, Australia (2013)
2013 Jiang C, Zhang XD, 'To keep PI3K/Akt in check in melanoma: more than just PTEN.', HCRA Translational Cancer Research Conference, HCRA Translational Cancer Research Conference (2013)
2013 Jiang C, Chi MN, Chen JZ, Ye Y, 'Adipocytes contribute to resistance of human melanoma cells to chemotherapy and targeted therapy', HCRA Translational Cancer Research Conference., Newcastle, Australia (2013)
2013 Liu YL, Lai F, Jiang C, Tseng HY, Jin L, Zhang XD, 'Noxa induced by oncogenic activation of MEK/ERK regulates autophagy in human melanoma.', HCRA Translational Cancer Research Conference., Newcastle, Australia (2013)
2013 Jin L, Dong L, Tseng HY, Wang CY, Wilmott JS, Yan XG, et al., 'Oncogenic suppression of PHLPP in human melanoma.', HCRA Translational Cancer Research Conference., Newcastle, Australia (2013)
2013 Wang CY, Jiang C, Tseng HY, Zhang XD, 'MicroRNA-497 targets insulin-like growth factor 1 receptor and has a tumour suppressive role in human colorectal cancer.', HCRA Translational Cancer Research Conference., Newcastle, Australia (2013)
2013 Liu XY, Lai F, Jiang C, Tseng HY, Jin L, Zhang XD, 'RIPK1 inhibition of killing by BRAF inhibitors in melanoma cells.', HCRA Translational Cancer Research Conference., Newcastle, Australia (2013)
2013 Tseng H-Y, Lai F, Jin L, Jiang CC, Kefford R, Long G, et al., 'Inhibition of Oncogenic BRAF Triggers Immunogenic Necrosis of Human Melanoma Cells', JOURNAL DER DEUTSCHEN DERMATOLOGISCHEN GESELLSCHAFT (2013) [E3]
Co-authors Lei Jin, Xu Zhang
2013 Liu H, Zhang Y-Y, Zhang Q-W, Chao Z-H, Zhang P, Jiang C-C, Jiang Z-W, '3-bromopyruvate induces necroptosis and autophagy in breast cancer cell lines', ACTA PHARMACOLOGICA SINICA (2013) [E3]
2012 Lai F, Jiang C, Hersey P, Zhang XD, 'Targeting histone deacetylases - a promising approach to improve therapeutic efficacy of mutant BRAF inhibitors in melanoma.', 24th Lorne Cancer Conference, Lorne, Australia (2012)
2012 Tseng HY, Chen LH, Ye Y, Tay KH, Jiang C, Hersey P, Zhang XD, 'The cancer testis antigen MAGED2 protects human melanoma cells from TRAIL-induced apoptosis by suppressing TRAIL-R2 expression.', 24th Lorne Cancer Conference, Lorne, Australia (2012)
2012 Jiang C, Guo ST, Wang GP, Tseng HY, Throne RF, Jin L, Zhang XD, 'MicroRNA-497 targets Insulin-like growth factor 1 receptor and has a tumor suppressive role in human colorectal cancer.', 6th Garvan Signaling Symposium, Sydney, Australia (2012)
2012 Tay KH, Jin L, Tseng HY, Jiang C, Ye Y, Throne RF, et al., 'Suppression of PP2A is critical for protection of melanoma cells upon endoplasmic reticulum stress.', 6th Garvan Signaling Symposium, Sydney, Australia (2012)
2012 Ye Y, Jin L, Wilmott JS, Hu WL, Yosufi B, Throne RF, et al., 'PI(4,5)P2 5-phosphatase A regulates PI3K/Akt signalling and has a tumour suppressive role in human melanoma.', Inaugural Melanoma Conference 2012, Perth, Australia (2012)
2012 Tseng H-Y, Chen LH, Ye Y, Jiang CC, Hersey P, Zhang XD, 'The cancer testis antigen MAGED2 protects human melanoma cells from TRAIL-induced apoptosis by suppressing TRAIL-R2 expression', CANCER RESEARCH (2012)
DOI 10.1158/1538-7445.AM2012-253
Co-authors Xu Zhang
2012 Tay KH, Tseng H-Y, Jing L, Jiang CC, Ye Y, Thorne R, et al., 'PP2A signaling is overridden by MEK/ERK activity leading to suppression of Bim and protection of melanoma cells from ER stress-induced apoptosis', CANCER RESEARCH (2012)
DOI 10.1158/1538-7445.AM2012-4990
Co-authors Xu Zhang, Rick Thorne
2011 Ye Y, Jin L, Wilmott J, Hu WL, Thorne RF, Dong L, et al., 'Phosphatidylinositol 4,5-Bisphosphate 5-Phosphatase A regulates PI3K/Akt signaling in human melanoma cells', Pigment Cell & Melanoma Research, Tampa, FL (2011) [E3]
DOI 10.1111/j.1755-148X.2011.00909.x
Co-authors Rick Thorne, Xu Zhang
2011 Hersey P, Wroblewski DJR, Lai FS, Jiang CC, Zhang XD, 'Targeting anti-apoptotic mechanisms for reversal of resistance to BRAF inhibitors in melanoma', Pigment Cell & Melanoma Research, Tampa, FL (2011) [E3]
DOI 10.1111/j.1755-148X.2011.00909.x
Co-authors Xu Zhang
2011 Ye Y, Dong L, Jiang C, Hersey P, Zhang XD, 'Epigenetic repression of the inoditol polyphosphate 5-Phosphatase PIPP contributes to activation of AKT and resistance to apoptosis in human melanoma.', 23rd Lorne Cancer Conference, Lorne, Australia (2011)
2011 Tseng HY, Jiang C, Croft A, Tay KH, Throne RF, Yang F, et al., 'P53 functions as a double-edged sword for response of human melanoma to treatment.', 23rd Lorne Cancer Conference, Lorne, Australia (2011)
2011 Wroblewski D, Jiang C, Croft A, Hersey P, Zhang XD, 'Activation of the unfolded protein response protects human melanoma cells against apoptosis induced by Obatoclax and ABT-737.', 23rd Lorne Cancer Conference, Lorne, Australia (2011)
2011 Croft A, Lai F, Jiang C, Hersey P, Zhang XD, 'Active XBP1 levels may predict resistance of B-RAF V600E melanoma cell lines to PLX4720', 23rd Lorne Cancer Conference, Lorne, Australia (2011)
2011 Tay KH, Jiang C, Tseng HY, Hersey P, Zhang XD, 'Dysregulation of the CHOP-Bim pathway contributes to resistance of melanoma cells to ER stress-induced apoptosis.', 23rd Lorne Cancer Conference, Lorne, Australia (2011)
2010 Dong L, Jiang CC, Thorne RF, Yang F, Liu H, De Bock CE, et al., 'Transcriptional up-regulation of Mcl-1 by ETS1 down-stream of XBP-1 in melanoma cells upon ER stress', Pigment Cell & Melanoma Research, Sydney, Australia (2010) [E3]
Co-authors Rick Thorne, Xu Zhang
2010 Chen LH, Yang F, Tay KH, Dong L, Thorne RF, Jiang CC, et al., 'Cystatin B inhibition of TRAIL-induced apoptosis is associated with protection of FLIPLfrom degradation by the E3 ligase itch human melanoma cells', Pigment Cell & Melanoma Research, Sydney, Australia (2010) [E3]
DOI 10.1038/cdd.2010.29
Co-authors Rick Thorne, Xu Zhang
2010 Yang XM, Chen LH, Jiang CC, De Bock CE, Thorne RF, Hersey P, Zhang XD, '40p53 is up-regulated and plays a role in antagonizing p53-mediated apoptosis in human melanoma', Pigment Cell & Melanoma Research, Sydney, Australia (2010) [E3]
Co-authors Rick Thorne, Xu Zhang
2010 Zhang XD, Jiang CC, Lai F, Croft A, Tay KH, Thorne RF, et al., 'Apoptotic response of mutant B-RAF human melanoma cells to a B-RAF inhibitor involves increased splicing production of BimS', AACR 101st Annual Meeting 2010. Abstracts, Washington, DC (2010) [E3]
Co-authors Xu Zhang, Rick Thorne
2010 Jiang CC, Zhuang LQ, Dong L, Thorne RF, Lavis CJ, Hersey P, Zhang XD, 'Adaptation to ER stress as a driver of increased expression of Mcl-1 with melanoma progression', AACR 101st Annual Meeting 2010. Abstracts, Washington, DC (2010) [E3]
Co-authors Rick Thorne, Xu Zhang
2010 Zhang XD, Jiang CC, Zhuang LQ, Hersey P, 'Adaptation to ER stress as a mechanism of resistance of melanoma to treatment', Melanoma 2010 Congress. Oral and Poster Abstracts, Sydney, NSW (2010) [E3]
Co-authors Xu Zhang
2010 Croft A, Lai F, Jiang CC, Zhang XD, Hersey P, 'Active XBP1 levels may predict resistance of B-Raf V600E melanoma cell lines to PLX4720', Melanoma 2010 Congress. Oral and Poster Abstracts, Sydney, NSW (2010) [E3]
Co-authors Xu Zhang
2010 Jiang CC, Lai FS, Hersey P, Zhang XD, 'Preferential splicing of BimS plays a predominant role in induction of apoptosis in human melanoma cells', Melanoma 2010 Congress. Oral and Poster Abstracts, Sydney, NSW (2010) [E3]
Co-authors Xu Zhang
2010 Lai F, Jiang CC, Hersey P, Zhang XD, 'Long-term exposure to the B-RAFV600E inhibitor PLX4720 results in melanoma cells with increased activation of ERK1/2 and high proliferation potential', Melanoma 2010 Congress. Oral and Poster Abstracts, Sydney, NSW (2010) [E3]
Co-authors Xu Zhang
2010 Tseng HY, Jiang CC, Croft A, Tay KH, Yang F, Liu H, et al., 'Contrasting effects of nutlin-3 on TRAIL- and docetaxel-induced apoptosis in human melanoma cells', Melanoma 2010 Congress. Oral and Poster Abstracts, Sydney, NSW (2010) [E3]
DOI 10.1158/1535-7163.MCT-10-0646
Citations Scopus - 24Web of Science - 24
Co-authors Xu Zhang, Rick Thorne
2010 Tay KH, Jiang CC, Tseng HY, Hersey P, Zhang XD, 'Rapid negative feedback regulation of CHOP contributes to resistance of melanoma cells to ER stress-induced apoptosis', Melanoma 2010 Congress. Oral and Poster Abstracts, Sydney, NSW (2010) [E3]
Co-authors Xu Zhang
2010 Zhang XD, Jiang C, Croft A, Lai F, Tay KH, Throne R, et al., 'Apoptosis response of mutant BRAF human melanoma cells to a BRAF inhibitor involves increased splicing production of BimS.', 101st Annual Meeting of American Association for Cancer Research, Washington DC, USA (2010)
2010 Jiang C, Zhang XD, Lucas K, Allen J, hersey P, 'Adaptation to ER stress as a driver of increased expression of Mcl-1 with melanoma progression', 101st Annual Meeting of American Association for Cancer Research,, Washington DC, USA. (2010)
2010 Zhang XD, Jiang C, Hersey P, 'Towards targeting adaptive mechanisms to ER stress in human melanoma', 22nd Lorne Cancer Conference, Lorne, Australia (2010)
2010 Lai F, Jiang C, Zhang XD, Hersey P, 'Human Melanoma Cells under Endoplasmic Reticulum Stress Are More Susceptible to Apoptosis Induced by the BH3 Mimetic Obatoclax,', 22nd Lorne Cancer Conference, Lorne, Australia (2010)
2010 Jiang C, Lai F, Hersey P, Zhang XD, 'Long-term exposure to the BRAFV600E inhibitor PLX4720 results in melanoma cells with increased activation of ERK1/2 and high proliferation potential.', 7th International Congress of the Society of melanoma research, Sydney, NSW, Australia (2010)
2010 Zhang XD, Jiang C, Lai F, Croft A, Tay KH, Throne RF, et al., 'Apoptosis response of mutant B-RAF human melanoma cells to a B-RAF inhibitor involves increased splicing production of BimS.', Cold Spring Harbor James Watson Cancer Symposium, Suzhou, China (2010)
2009 Kiejda KA, Scurr LL, Wade MA, Jiang CC, Weir AJW, Bowden NA, et al., 'Cisplatin induces apoptosis independently of Noxa or PUMA in human melanoma cells', 21st Lorne Cancer Conference, Lorne, VIC (2009) [E3]
Co-authors Nikola Bowden, Xu Zhang, Rodney Scott, Kelly Kiejda
2009 Wroblewski D, Jiang C, Mao ZG, Zhang XD, Hersey P, 'Multiple mechanisms are responsible for killing of human melanoma cells by the BH3 mimetic Obatoclax', 21st Lorne Cancer Conference, Lorne, Australia (2009)
2009 Yang F, Jiang C, Yang E, Christopherson R, Crossett B, Elias R, Hersey P, 'Cystatin B protects human melanoma cells against TRAIL-induced apoptosis by inhibiting activation of Caspase-8.', 21st Lorne Cancer Conference, Lorne, Australia (2009)
2009 Jiang C, Zhang XD, Hersey P, 'XBP1 up-regulates Mcl-1 via activation of AKT in human melanoma cells under ER stress.', 21st Lorne Cancer Conference, Lorne, Australia (2009)
2009 Weir AJW, Jiang C, Mao Z, Throne RF, Zhu B, Hersey P, Zhang XD, 'Human melanoma cells under Endoplasmic Reticulum stress acquire resistance to microtubule-targeting drugs.', 21st Lorne Cancer Conference, Lorne, Australia (2009)
2009 Zhang XD, Jiang C, Chen LH, Hersey P, 'Towards targeting adaptive mechanisms of ER stress in human melanoma.', 21st Lorne Cancer Conference., Lorne, Australia (2009)
2009 Lavis C, Jiang C, Zhang XD, Hersey P, 'CHOP mediated apoptotic signalling is non-functional in melanoma under Endoplasmic Reticulum Stress.', 21st Lorne Cancer Conference., Lorne, Australia (2009)
2009 Zhang XD, Jiang CC, Thorne R, Lucas K, Allen J, Hersey P, 'Up-regulation of Mcl-1 via XBP1-mediated activation of Akt is critical for survival of melanoma cells upon ER stress', CANCER RESEARCH (2009)
Co-authors Xu Zhang, Rick Thorne
2008 Zhang XD, Jiang CC, Avery-Kiejda KA, Lucas K, Wade M, Allen J, Hersey P, 'Up-regulation of Mcl-1 by the unfolded protein response is critical for survival of melanoma cells upon ER stress', PIGMENT CELL & MELANOMA RESEARCH (2008) [E3]
Co-authors Xu Zhang, Kelly Kiejda
2008 Jiang CC, Wade MA, Kiejda KA, Wang Y, Zhang XD, Hersey P, 'Up-regulation of MCL-1 is critical for survival of human melanoma cells upon ER stress', 20th Lorne Cancer Conference, Lorne, VIC (2008) [E3]
Co-authors Xu Zhang, Kelly Kiejda
2008 Zhang XD, Jiang CC, Wang YF, Kiejda KA, Hersey P, 'The MEK/ERK pathway potentiates adaptation of human melanoma to endoplasmic reticulum stress', 20th Lorne Cancer Conference, Lorne, VIC (2008) [E3]
Co-authors Xu Zhang, Kelly Kiejda
2008 Zhang XD, Jiang C, Chen LH, Kiejda KA, Wade M, Hersey P, 'Multiple apoptosis pathways are inhibited in human melanoma cells upon ER stress.', 16th Euroconference on Apoptosis, Bern, Switzerland (2008)
2008 Jiang C, Zhang XD, Wang YF, Kiejda KA, Hersey P, 'The MEK/ERK Pathway Potentiates Adaptation of Human Melanoma to Endoplasmic Reticulum Stress', 20th Lorne Cancer Conference, Lorne, Australia (2008)
2008 Jiang C, Wang YF, Kiejda KA, Zhang XD, Hersey P, 'The MEK/ERK pathway potentiates adaptation of human melanoma to endoplasmic reticulum stress.', 99th Annual Meeting of American Association for Cancer Research, San Diego, USA (2008)
2008 Zhang XD, Jiang C, Wang YF, Wade M, Kiejda KA, Hersey P, 'The unfolded protein response differentially regulates sensitivities of human melanoma cells to chemotherapeutic drugs.', 99th Annual Meeting of American Association for Cancer Research, San Diego, USA (2008)
2008 Lavis C, Jiang C, Zhang XD, Hersey P, 'CHOP mediated apoptotic signalling is non-functional in melanoma under Endoplasmic Reticulum Stress.', HMRI Conference on Translational Cancer Research, Newcastle, Australia (2008)
2008 Wroblewski D, Jiang C, Mao ZG, Zhang XD, Hersey P, 'Multiple mechanisms are responsible for killing of human melanoma cells by the BH3 mimetic Obatoclax.', HMRI Conference on Translational Cancer Research, Newcastle, Australia (2008)
2008 Jiang C, Zhang XD, Hersey P, 'The MEK/ERK pathway potentiates adaptation of human melanoma to endoplasmic reticulum stress', HMRI Conference on Translational Cancer Research, Newcastle, Australia (2008)
2007 Hersey P, Zhang XD, Jiang CC, Chen LH, 'Endoplasmic stress (ER) in melanoma cells', Archives of Dermatological Research, Barcelona, Spain (2007) [E3]
Co-authors Xu Zhang
2007 Jiang CC, Chen IH, Kiejda KA, Gillespie SK, Hersey P, Zhang XD, 'The unfolded protein response induced by tunicamycin or thapsigargin sensitizes human melanoma cells to trail-induced apoptosis by selective up-regulaton of trail-R2 on te cell surface', 19th Lorne Cancer Conference, Lorne, VIC (2007) [E3]
Co-authors Xu Zhang, Kelly Kiejda
2007 Zhang XD, Jiang CC, Wang YF, Kiejda KA, Gillespie SK, Hersey P, 'Regulation of the BCL-2 family members BIM, PUMA and MCL-1 by MEK/ERK signaling plays a critical role in survival of melanoma cells', 19th Lorne Cancer Conference, Lorne, VIC (2007) [E3]
Co-authors Kelly Kiejda, Xu Zhang
2007 Zhang XD, Jiang CC, Wang YF, Kiejda KA, Hersey P, 'The MEK-ERK pathway potentiates adaptation of melanoma to endoplasmic reticulum stress', 4th Garvan Signalling Symposium. Conference Proceedings, Sydney, NSW (2007) [E3]
Co-authors Kelly Kiejda, Xu Zhang
2007 Jiang CC, Wang YF, Kiejda KA, Gillespie SK, Zhang XD, Hersey P, 'Regulation of the Bcl-2 family members Bim, PUMA and Mcl-1 by MEK/ERK signaling plays a critical role in survival of melanoma cells', AACR Meeting Abstracts Online (Abstracts of the 98th AACR Annual Meeting), Los Angeles (2007) [E3]
Co-authors Xu Zhang, Kelly Kiejda
2007 Jiang C, Wang YF, Kiejda KA, Zhang XD, Hersey P, 'MEK/ERK-mediated regulation of the Bcl-2 family members Mcl-1, PUMA, and Bim contributes to survival of human melanoma cells', 4th Garvan Signaling Symposium, Sydney, NSW, Australia (2007)
2007 Jiang C, Wang YF, Kiejda KA, Zhang XD, Hersey P, 'Apoptosis induction by inhibition of MEK is mediated by the Bcl-2 family members Bim, PUMA and Mcl-1.', 98th Annual Meeting of American Association for Cancer Research, Los Angeles, USA (2007)
2007 Zhang XD, Jiang C, Chen LH, Kiejda KA, Hersey P, 'The unfolded protein response selectively up-regulates TRAIL-R2 and enhances TRAIL-induced apoptosis in human melanoma cells.', 98th Annual Meeting of American Association for Cancer Research, Los Angeles, USA (2007)
2006 Jiang CC, Wang YF, Kiejda KA, Zhang XD, Hersey P, 'CD133, A potential marker for cancer stem cells in melanoma', HMRI Conference on Translational Cancer Research. Molecular Mechanisms and Implications for Treatment, Newcastle, NSW (2006) [E3]
Co-authors Xu Zhang, Kelly Kiejda
2006 Wang YF, Jiang CC, Kiejda KA, Zhang XD, Hersey P, 'Suppression of the BH3-only proteins BUM and PUMA by MEK/ERK signaling plays a crucial role in maintaining survival of melanoma cells', HMRI Conference on Translational Cancer Research. Molecular Mechanisms and Implications for Treatment, Newcastle, NSW (2006) [E3]
Co-authors Xu Zhang, Kelly Kiejda
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Grants and Funding

Summary

Number of grants 28
Total funding $3,325,311

Click on a grant title below to expand the full details for that specific grant.


20171 grants / $25,000

Epigenetic control of transcriptional activation of PDL1 by a HOXA5/STAT3 complex in cancer cells by a HOXA5/STAT3 complex in cancer cells$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Chen Chen Jiang, Professor Xu Dong Zhang, Doctor Lei Jin
Scheme Project Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1700351
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20157 grants / $1,185,095

Overcoming Resistance of Metastatic Melanoma to treatment: MicroRNA-dependent expression of INPP4B as a biomarker and therapeutic target in melanoma$598,176

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Doctor Chen Chen Jiang
Scheme Career Development Fellowship
Role Lead
Funding Start 2015
Funding Finish 2017
GNo G1400739
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Advanced Technical Support for Oncology Single Cell Analysis Technologies$300,000

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Laureate Professor Rodney Scott, Professor Xu Dong Zhang, Professor Hubert Hondermarck, Conjoint Professor Stephen Ackland, Doctor Craig Gedye, Doctor Pradeep Tanwar, Doctor Chen Chen Jiang, Doctor Matt Dun, Professor Paul de Souza, Associate Professor Kevin Spring, Dr Tao Liu
Scheme Research Infrastructure Grants
Role Investigator
Funding Start 2015
Funding Finish 2018
GNo G1500824
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

Necropotosis induced by Hexokinase-II inhibitor in breast cancer$150,555

Funding body: The National Natural Science Fund

Funding body The National Natural Science Fund
Project Team

Hao Liu

Scheme The National Natural Science Fund
Role Investigator
Funding Start 2015
Funding Finish 2017
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

Development of tumor cells energy metabolism based necropotosis inhibitor$66,666

Funding body: Foreign cooperation project grant in science and technology

Funding body Foreign cooperation project grant in science and technology
Scheme Foreign cooperation project grant in science and technology
Role Lead
Funding Start 2015
Funding Finish 2017
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

High throughput automated all-in-one laser scanning FLUOVIEW FV10i microscope$54,698

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Xu Dong Zhang, Professor Robert Callister, Laureate Professor John Aitken, Doctor Pradeep Tanwar, Doctor Chen Chen Jiang, Doctor Lei Jin
Scheme Equipment Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1501576
Type Of Funding Other Public Sector - Commonwealth
Category 2OPC
UON Y

The Long non-coding RNA lnc-DAGLA-1 as a biomarker and therapeutic target in melanoma. $10,000

Funding body: Faculty of Health, University of Newcastle

Funding body Faculty of Health, University of Newcastle
Project Team

Lei Jin

Scheme Strategic Research Pilot Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo
Type Of Funding Internal
Category INTE
UON N

Co-targeting CD47 and PD-L1 to enhance the efficacy of immunotherapy in melanoma.$5,000

Funding body: Faculty of Health, University of Newcastle

Funding body Faculty of Health, University of Newcastle
Scheme Strategic Research Pilot Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo
Type Of Funding Internal
Category INTE
UON N

20141 grants / $20,000

Overcoming resistance of KRAS mutant colon cancer to treatment by targeting heat shock protein 90$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Chen Chen Jiang, Professor Xu Dong Zhang
Scheme Project Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1401417
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20134 grants / $898,657

Functional consequences of epigenetic repression of PIB5PA in melanoma$359,253

Funding body: Cancer Council NSW

Funding body Cancer Council NSW
Project Team Professor Xu Dong Zhang, Dr Helen Rizos, Doctor Rick Thorne, Doctor Chen Chen Jiang
Scheme Research Grant
Role Investigator
Funding Start 2013
Funding Finish 2016
GNo G1200386
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Targeting PP2A to improve the therapeutic efficacy of mutant BRAF inhibitors in melanoma$359,253

Funding body: Cancer Council NSW

Funding body Cancer Council NSW
Project Team Professor Xu Dong Zhang, Doctor Nikki Verrills, Doctor Chen Chen Jiang
Scheme Research Grant
Role Investigator
Funding Start 2013
Funding Finish 2016
GNo G1200388
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Targeting microRNA-768-3p to overcome the resistance of human nasopharyngeal carcinoma cells to treatment. $155,555

Funding body: The National Natural Science Fund

Funding body The National Natural Science Fund
Scheme The National Natural Science Fund
Role Lead
Funding Start 2013
Funding Finish 2017
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

20125 grants / $430,974

Targeting Histone Deacetylases to Overcome Resistance of BRAFV600E Melanoma Cells to Apoptosis$346,974

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Xu Dong Zhang, Conjoint Professor Peter Hersey, Dr Tao Liu, Doctor Chen Chen Jiang, Doctor Rick Thorne
Scheme Project Grant
Role Investigator
Funding Start 2012
Funding Finish 2014
GNo G1100133
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

The Role of Phosphatidylinositol 4, 5-Bisphosphate 5-Phosphatase A (PIB5PA) in Regulation of PI3K/Akt Signalling in Melanoma$24,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Xu Dong Zhang, Doctor Chen Chen Jiang
Scheme Project Grant
Role Investigator
Funding Start 2012
Funding Finish 2012
GNo G1101121
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

A p53-Mediated Pro-Survival Signaling Pathway in Human Melanoma Progression and Resistance to Treatment$20,000

Funding body: University of Newcastle

Funding body University of Newcastle
Project Team Professor Xu Dong Zhang, Doctor Rick Thorne, Doctor Chen Chen Jiang
Scheme Near Miss Grant
Role Investigator
Funding Start 2012
Funding Finish 2012
GNo G1200672
Type Of Funding Internal
Category INTE
UON Y

Targeting ER stress to sensitize head and neck and maxillofacial tumor cells to chemotherapeutic reagents$20,000

Funding body: The Natural Science Foundation of Anhui Province

Funding body The Natural Science Foundation of Anhui Province
Project Team

Jing Cheng Xu, Zhi Wen Jiang, Hao Liu

Scheme The Natural Science Foundation of Anhui Province
Role Investigator
Funding Start 2012
Funding Finish 2013
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

Biological polysaccharide anti-tumor drug research collaborative innovation centre$20,000

Funding body: Bengbu Medical College

Funding body Bengbu Medical College
Project Team

Zhi Wen Jiang, Hao Liu

Scheme Bengbu Medical College
Role Investigator
Funding Start 2012
Funding Finish 2012
GNo
Type Of Funding Not Known
Category UNKN
UON N

20114 grants / $487,253

Targeting survival pathways to overcome the resistance of human melanoma to treatment$320,032

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Doctor Chen Chen Jiang
Scheme Training (Postdoctoral) Fellowships - Peter Doherty Biomedical Fellowship (Australia)
Role Lead
Funding Start 2011
Funding Finish 2014
GNo G1000530
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

The role of Endoplasmic Reticulum stress in regulating sensitivity of human nasopharyngeal carcinoma cells to chemotherapy$75,555

Funding body: The National Natural Science Fund

Funding body The National Natural Science Fund
Scheme The National Natural Science Fund
Role Lead
Funding Start 2011
Funding Finish 2013
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

The role of RIPK1 in regulating sensitivity of tumor cells to SMAC mimetic-induced cell death$66,666

Funding body: The National Natural Science Fund

Funding body The National Natural Science Fund
Project Team

Hao Liu

Scheme The National Natural Science Fund
Role Investigator
Funding Start 2011
Funding Finish 2013
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

Regulation of BimS splicing in response of human melanoma cells to inhibition of BRAFVV600E$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Chen Chen Jiang, Professor Xu Dong Zhang
Scheme Project Grant
Role Lead
Funding Start 2011
Funding Finish 2011
GNo G1000988
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

20104 grants / $145,000

MicroRNAs in adaptation of human melanoma cells to endoplasmic reticulum stress$90,000

Funding body: Cure Cancer Australia Foundation

Funding body Cure Cancer Australia Foundation
Project Team Doctor Chen Chen Jiang
Scheme Research Grant
Role Lead
Funding Start 2010
Funding Finish 2011
GNo G0190493
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Regulation of BimS splicing in response of human melanoma cells to inhibition of mutant BRAF.$25,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Scheme Project Grant
Role Lead
Funding Start 2010
Funding Finish 2010
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

The role of micro-RNA-149 in Regulation of Mcl-1 in Human Melanoma under stress$20,000

Funding body: Hunter Children`s Research Foundation

Funding body Hunter Children`s Research Foundation
Project Team Doctor Chen Chen Jiang, Professor Xu Dong Zhang
Scheme Research Grant
Role Lead
Funding Start 2010
Funding Finish 2010
GNo G0900189
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

The role of microRNA-149* in regulation of Mcl-1 in human melanoma under ER stress. $10,000

Funding body: Calvary Mater Newcastle Hospital

Funding body Calvary Mater Newcastle Hospital
Scheme Margaret Mitchell Research Grant
Role Lead
Funding Start 2010
Funding Finish 2010
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

20092 grants / $133,332

The role of heparan sulfate proteoglycan in regulating sensitivity of breast cancer cells to ER-stress induced cell death$66,666

Funding body: The Natural Science Foundation of Anhui Province

Funding body The Natural Science Foundation of Anhui Province
Project Team

Zhi Wen Jiang, Hao Liu

Scheme The Natural Science Foundation of Anhui Province
Role Investigator
Funding Start 2009
Funding Finish 2011
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N

R & D of heparin structure modification and anti-tumor effects$66,666

Funding body: The Natural Science Foundation of Anhui Province

Funding body The Natural Science Foundation of Anhui Province
Project Team

Zhi Wen Jiang, Hao Liu

Scheme The Natural Science Foundation of Anhui Province
Role Investigator
Funding Start 2009
Funding Finish 2011
GNo
Type Of Funding International - Competitive
Category 3IFA
UON N
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Research Supervision

Number of supervisions

Completed3
Current3

Total current UON EFTSL

Masters0.2
PhD0.9

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2016 Masters Oncogenic Upregulation for the Long Noncoding RNA MAFG-AS1 M Philosophy (Medical Biochem), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2014 PhD The significance of INPP4B upregulation in the pathogenesis of colon cancer PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
2014 PhD Targeting Heat Shock Protein 90 in Human Colon Cancer PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2014 PhD Targeting Adaptive Mechanisms to Endoplasmic Reticulum Stress in Melanoma Surgery, Faculty of Health, University of Newcastle Co-Supervisor
2014 PhD Inositol Polyphosphate 4-Phosphatese 11 (INPP4B) Promotes PI3K Signalling and Functions as an Oncogenic Regulator in Human Colon Cancer and Melanoma Surgery, Faculty of Health, University of Newcastle Co-Supervisor
2014 PhD Regulation of Apoptosis Induced by Targeting the RAF/MEK/ERK Pathway in Human Melanoma PhD (Surgical Science), Faculty of Health and Medicine, The University of Newcastle Co-Supervisor
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Research Collaborations

The map is a representation of a researchers co-authorship with collaborators across the globe. The map displays the number of publications against a country, where there is at least one co-author based in that country. Data is sourced from the University of Newcastle research publication management system (NURO) and may not fully represent the authors complete body of work.

Country Count of Publications
Australia 92
China 67
United States 4
United Kingdom 2
France 1
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Dr Chen Chen Jiang

Positions

Cancer Institute NSW Career Development Fellow
School of Medicine and Public Health
Faculty of Health and Medicine

Casual Lecturer
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Contact Details

Email chenchen.jiang@newcastle.edu.au
Phone (02) 4921 7233
Mobile N/A
Fax (02) 4921 7311

Office

Room LS3-38
Building Life Sciences Building
Location Callaghan
University Drive
Callaghan, NSW 2308
Australia
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