2023 |
Hondermarck H, Jiang CC, 'Time to Introduce Nerve Density in Cancer Histopathologic Assessment', CLINICAL CANCER RESEARCH, 29 2342-2344 (2023)
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Nova |
2023 |
Wang Y, Jiang C, Tang M, Li H, Zhao C, Zhao M, et al., 'Effective clinical response of lung adenocarcinoma harboring
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2023 |
Dowdell A, Marsland M, Faulkner S, Gedye C, Lynam J, Griffin CP, et al., 'Targeting XBP1 mRNA splicing sensitizes glioblastoma to chemotherapy', FASEB BIOADVANCES, 5 211-220 (2023) [C1]
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Nova |
2023 |
Marsland M, Dowdell A, Faulkner S, Gedye C, Lynam J, Griffin CP, et al., 'The Membrane Protein Sortilin Is a Potential Biomarker and Target for Glioblastoma', Cancers, 15 2514-2514 [C1]
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Nova |
2023 |
Tang M, Li X, Zhang Y, Li H, Zhao C, Zhao M, et al., 'Effective treatment of MET-amplified non-small cell lung cancer patients with crizotinib: a case description', QUANTITATIVE IMAGING IN MEDICINE AND SURGERY, 13 3351-3356 (2023)
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2023 |
Marsland M, Dowdell A, Faulkner S, Jobling P, Rush RA, Gedye C, et al., 'ProNGF Expression and Targeting in Glioblastoma Multiforme.', Int J Mol Sci, 24 (2023) [C1]
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Nova |
2022 |
Zhao M, Wang Y, Zhang Y, Li X, Mi J, Wang Q, et al., 'The upregulation of stromal antigen 3 expression suppresses the phenotypic hallmarks of hepatocellular carcinoma through the Smad3-CDK4/CDK6-cyclin D1 and CXCR4/RhoA pathways.', BMC Gastroenterol, 22 378 (2022) [C1]
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Nova |
2022 |
Jiang CC, Marsland M, Wang Y, Dowdell A, Eden E, Gao F, et al., 'Tumor innervation is triggered by endoplasmic reticulum stress', ONCOGENE, 41 586-599 (2022) [C1]
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Nova |
2022 |
Li X, Liu H, Dun MD, Faulkner S, Liu X, Jiang CC, Hondermarck H, 'Proteome and secretome analysis of pancreatic cancer cells', PROTEOMICS, 22 (2022) [C1]
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Nova |
2022 |
Wang Y, Zhang Y, Mi J, Jiang C, Wang Q, Li X, et al., 'ANKFN1 plays both protumorigenic and metastatic roles in hepatocellular carcinoma', ONCOGENE, 41 3680-3693 (2022) [C1]
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Nova |
2022 |
Hong X, Li D, Yang X, Fu G, Jiang C, Zhang W, 'Nomogram for Predicting the Severity of Coronary Artery Disease in Young Adults =45 Years of Age with Acute Coronary Syndrome', CARDIOVASCULAR INNOVATIONS AND APPLICATIONS, 7 (2022) [C1]
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2022 |
Marsland M, Dowdell A, Jiang CC, Wilmott JS, Scolyer RA, Zhang XD, et al., 'Expression of NGF/proNGF and Their Receptors TrkA, p75(NTR) and Sortilin in Melanoma', INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 23 (2022) [C1]
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Nova |
2021 |
Zhao M, Wang Y, Jiang C, Wang Q, Mi J, Zhang Y, et al., 'miR-107 regulates the effect of MCM7 on the proliferation and apoptosis of colorectal cancer via the PAK2 pathway', BIOCHEMICAL PHARMACOLOGY, 190 (2021) [C1]
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Nova |
2021 |
Li J, Pang J, Liu Z, Ge X, Zhen Y, Jiang CC, et al., 'Shikonin induces programmed death of fibroblast synovial cells in rheumatoid arthritis by inhibiting energy pathways', SCIENTIFIC REPORTS, 11 (2021) [C1]
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Nova |
2021 |
Ferdoushi A, Griffin N, Marsland M, Xu X, Faulkner S, Gao F, et al., 'Tumor innervation and clinical outcome in pancreatic cancer', SCIENTIFIC REPORTS, 11 (2021) [C1]
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Nova |
2021 |
Cheng X, Liu H, Jiang CC, Fang L, Chen C, Zhang XD, Jiang ZW, 'Retraction: Connecting endoplasmic reticulum stress to autophagy through IRE1/JNK/beclin-1 in breast cancer cells (International Journal of Molecular Medicine (2014) 34 (772-781) DOI: 10.3892/ijmm.2014.1822)', International Journal of Molecular Medicine, 48 (2021)
Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that possible anomalies were associated with data shown in Fig. 4B, C an... [more]
Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that possible anomalies were associated with data shown in Fig. 4B, C and E, and western blotting data shown in Fig. 5, such that it was difficult to interpret the presented results as having originated from discrete experiments performed in two breast cancer cell lines (MCF-7 and MDA-MB-231). After having investigated the matter internally, the Editor of International Journal of Molecular Medicine has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory response. The Editor apologizes to the readership for any inconvenience caused.
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2021 |
Li Y, Liu H, Huang YY, Pu LJ, Zhang XD, Jiang CC, Jiang ZW, 'Erratum: Suppression of endoplasmic reticulum stress-induced invasion and migration of breast cancer cells through the downregulation of heparanase (Int J Mol Med (2013) 31 (1234-1242) DOI: 10.3892/ijmm.2013.1292)', International Journal of Molecular Medicine, 48 (2021)
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2020 |
Ferdoushi A, Li X, Griffin N, Faulkner S, Jamaluddin MFB, Gao F, et al., 'Schwann Cell Stimulation of Pancreatic Cancer Cells: A Proteomic Analysis', Frontiers in Oncology, 10 (2020) [C1]
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Nova |
2020 |
Gao F, Griffin N, Faulkner S, Li X, King SJ, Jobling P, et al., 'The Membrane Protein Sortilin Can Be Targeted to Inhibit Pancreatic Cancer Cell Invasion.', The American journal of pathology, 190 (2020) [C1]
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Nova |
2020 |
Liu H, Li X, Dun MD, Faulkner S, Jiang CC, Hondermarck H, 'Cold Shock Domain Containing E1 (CSDE1) Protein is Overexpressed and Can be Targeted to Inhibit Invasiveness in Pancreatic Cancer Cells', PROTEOMICS, 20 (2020) [C1]
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Nova |
2019 |
Faulkner S, Jobling P, March B, Jiang CC, Hondermarck H, 'Tumor neurobiology and the war of nerves in cancer', Cancer Discovery, 9 702-710 (2019) [C1]
Nerves are emerging regulators of cancer progression. Cancer cells induce the outgrowth of nerves in the tumor microenvironment through the release of neu-rotrophic factors, and i... [more]
Nerves are emerging regulators of cancer progression. Cancer cells induce the outgrowth of nerves in the tumor microenvironment through the release of neu-rotrophic factors, and in return nerves liberate neurotransmitters that activate cancer growth and dissemination. Although sympathetic nerves drive tumor angiogenesis via the liberation of noradrena-line, sensory and parasympathetic nerves stimulate cancer stem cells. Interestingly, recent evidence indicates that parasympathetic nerves can eventually inhibit tumor progression, suggesting a yin¿yang type of regulation of cancer by nerves. From a broader perspective, the question of a higher level of control of cancer development by the central nervous system should be raised. Significance: Nerves are emerging regulators of cancer initiation, progression, and metastasis. Here, we review the evidence to date and explore the basic and clinical ramifications of these findings.
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Nova |
2019 |
Wong M, Sun Y, Xi Z, Milazzo G, Poulos RC, Bartenhagen C, et al., 'JMJD6 is a tumorigenic factor and therapeutic target in neuroblastoma', NATURE COMMUNICATIONS, 10 (2019) [C1]
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Nova |
2018 |
Wang YF, Liu F, Sherwin S, Farrelly M, Yan XG, Croft A, et al., 'Cooperativity of HOXA5 and STAT3 Is Critical for HDAC8 Inhibition-Mediated Transcriptional Activation of PD-L1 in Human Melanoma Cells', Journal of Investigative Dermatology, 138 922-932 (2018) [C1]
Although the expression of programmed death-ligand 1 (PD-L1) is an important mechanism by which cancer cells evade the immune system, PD-L1 expression in cancer cells is commonly ... [more]
Although the expression of programmed death-ligand 1 (PD-L1) is an important mechanism by which cancer cells evade the immune system, PD-L1 expression in cancer cells is commonly associated with patients¿ responses to treatment with anti-programmed death 1/PD-L1 antibodies. However, how PD-L1 expression is regulated in melanoma cells remains to be fully elucidated. Here we report that the class I histone deacetylase (HDAC) HDAC8 controls transcriptional activation of PD-L1 by a transcription complex consisting of transcription factors homeobox A5 and signal transducer and activator of transcription 3. Inhibition of HDAC8 upregulated PD-L1 in melanoma cells. This was due to an increase in the activity of a fragment of the PD-L1 gene promoter that is enriched with binding sites for both homeobox A5 and signal transducer and activator of transcription 3. Indeed, knockdown of homeobox A5 or signal transducer and activator of transcription 3 abolished upregulation of PD-L1 by HDAC8 inhibition. Moreover, homeobox A5 and signal transducer and activator of transcription 3 were physically associated and appeared interdependent in activating PD-L1 transcription. Functional studies showed that HDAC8-mediated regulation of PD-L1 expression participated in modulating anti-melanoma T-cell responses. Collectively, these results identify HDAC8 as an important epigenetic regulator of PD-L1 expression, with implications for better understanding of the interaction between melanoma cells and the immune system.
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Nova |
2018 |
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', Molecular Carcinogenesis, 57 284-294 (2018) [C1]
Past studies have shown that mutant KRAS colon cancer cells are susceptible to apoptosis induced by the HSP90 inhibitor AUY922. Nevertheless, intrinsic and acquired resistance rem... [more]
Past studies have shown that mutant KRAS colon cancer cells are susceptible to apoptosis induced by the HSP90 inhibitor AUY922. Nevertheless, intrinsic and acquired resistance remains an obstacle for the potential application of the inhibitor in the treatment of the disease. Here we report that Mcl-1 is important for survival of colon cancer cells in the presence of AUY922. Mcl-1 was upregulated in mutant KRAS colon cancer cells selected for resistance to AUY922-induced apoptosis. This was due to its increased stability mediated by Bcl-2-associated athanogene domain 3 (BAG3), which was also increased in resistant colon cancer cells by heat shock factor 1 (HSF1) as a result of chronic endoplasmic reticulum (ER) stress. Functional investigations demonstrated that inhibition of Mcl-1, BAG3, or HSF1 triggered apoptosis in resistant colon cancer cells, and rendered AUY922-naïve colon cancer cells more sensitive to the inhibitor. Together, these results identify that the HSF1-BAG3-Mcl-1 signal axis is critical for protection of mutant KRAS colon cancer cells from AUY922-induced apoptosis, with potential implications for targeting HSF1/BAG3/Mcl-1 to improve the efficacy of AUY922 in the treatment of colon cancer.
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Nova |
2018 |
Faulkner S, Jobling P, Rowe CW, Rodrigues Oliveira SM, Roselli S, Thorne RF, et al., 'Neurotrophin Receptors TrkA, p75
Neurotrophin receptors are emerging targets in oncology, but their clinicopathologic significance in thyroid cancer is unclear. In this study, the neurotrophin tyrosine receptor k... [more]
Neurotrophin receptors are emerging targets in oncology, but their clinicopathologic significance in thyroid cancer is unclear. In this study, the neurotrophin tyrosine receptor kinase TrkA (also called NTRK1), the common neurotrophin receptor p75NTR, and the proneurotrophin receptor sortilin were analyzed with immunohistochemistry in a cohort of thyroid cancers (n = 128) and compared with adenomas and normal thyroid tissues (n = 62). TrkA was detected in 20% of thyroid cancers, compared with none of the benign samples (P = 0.0007). TrkA expression was independent of histologic subtypes but associated with lymph node metastasis (P = 0.0148), suggesting the involvement of TrkA in tumor invasiveness. Nerves in the tumor microenvironment were positive for TrkA. p75NTR was overexpressed in anaplastic thyroid cancers compared with papillary and follicular subtypes (P < 0.0001). Sortilin was overexpressed in thyroid cancers compared with benign thyroid tissues (P < 0.0001). Neurotrophin receptor expression was confirmed in a panel of thyroid cancer cell lines at the mRNA and protein levels. Functional investigations using the anaplastic thyroid cancer cell line CAL-62 found that siRNA against TrkA, p75NTR, and sortilin decreased cell survival and cell migration through decreased SRC and ERK activation. Together, these data reveal TrkA, p75NTR, and sortilin as potential therapeutic targets in thyroid cancer.
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Nova |
2018 |
Sun XJ, Ma LY, Zhang MX, Wang Y, Zhang P, Jiang CC, Liu H, 'Chloroquine induces apoptosis of human hepatocellular carcinoma cells in vitro by miR-26b-mediated regulation of Mcl-1', Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 38 409-413 (2018)
OBJECTIVE: To investigate the effect of chloroquine in inducing apoptosis of human hepatocellular carcinoma cells and explore the possible mechanism. METHODS: MTT assay and flow c... [more]
OBJECTIVE: To investigate the effect of chloroquine in inducing apoptosis of human hepatocellular carcinoma cells and explore the possible mechanism. METHODS: MTT assay and flow cytometry were used to evaluate chloroquine-induced growth inhibition and apoptosis in human hepatocellular carcinoma HepG2 cells, respectively. The ATP levels in chloroquine-treated cells were detected using an ATP assay kit. PCR and Western blotting were used to detect the expression levels of miR-26b and Mcl-1 in the cells, respectively. RESULTS: Chloroquine inhibited the proliferation of HepG2 cells in a time- and concentration-dependent manner. Treatments with 80 µmol/L chloroquine for 24, 48, and 72 h induced survival rates of (71.59±0.2)%, (45.40±0.5)%, and (26.34±1.4)% in the cells. Treatments with chloroquine at 40, 80, and 160 µmol/L for 5 h resulted in obviously lowered intracellular ATP levels in the cells to 87.80%, 71.29%, and 38.02% of the control level, respectively. At 80 µmol/L, chloroquine significantly increased the expression of miR-26b and down-regulated the expression of Mcl-1 in HepG2 cells, and the application of the miR-26b inhibitor increased the cellular expression of Mcl-1. CONCLUSION: s Chloroquine can inhibit the cell proliferation, reduce ATP level and induce apoptosis in HepG2 cells possibly through miR-26b-mediated regulation of Mcl-1.
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2018 |
Zhang YY, Tabataba H, Liu XY, Wang JY, Yan XG, Farrelly M, et al., 'ACTN4 regulates the stability of RIPK1 in melanoma', ONCOGENE, 37 4033-4045 (2018) [C1]
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Nova |
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]
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 kina... [more]
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.
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Nova |
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]
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Nova |
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) [C1]
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Nova |
2017 |
Li QX, Zhang P, Liu F, Wang XZ, Li L, Wang ZK, et al., 'Monocarboxylate transporter 1 enhances the sensitivity of breast cancer cells to 3-bromopyruvate in vitro', Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 37 588-593 (2017)
OBJECTIVE: To investigate the role of monocarboxylate transporter 1 (MCT1) in enhancing the sensitivity of breast cancer cells to 3-bromopyruvate (3-BrPA). METHODS: The inhibitory... [more]
OBJECTIVE: To investigate the role of monocarboxylate transporter 1 (MCT1) in enhancing the sensitivity of breast cancer cells to 3-bromopyruvate (3-BrPA). METHODS: The inhibitory effect of 3-BrPA on the proliferation of breast cancer cells was assessed with MTT assay, and brominated propidium bromide single staining flow cytometry was used for detecting the cell apoptosis. An ELISA kit was used to detect the intracellular levels of hexokinase II, lactate dehydrogenase, lactate, and adenosine triphosphate, and Western blotting was performed to detect the expression of MCT1. MDA-MB-231 cells were transiently transfected with MCT1 cDNA for over-expressing MCT1, and the effect of 3-BrPA on the cell proliferation and adenosine triphosphate level was deteced. RESULTS: 3-BrPA did not produce significant effects on the proliferation and apoptosis of MDA-MB-231 cells, and the cells treated with 200 µmol/L 3-BrPA for 24 h showed an inhibition rate and an apoptosis rate of only 8.72% and 7.8%, respectively. The same treatment, however, produced an inhibition rate and an apoptosis rate of 84.6% and 82.3% in MCF-7 cells, respectively. In MDA-MB-231 cells with MCT1 overexpression, 200 µmol/L 3-BrPA resulted in an inhibition rate of 72.44%, significantly higher than that in the control cells (P<0.05); treatment of the cells with 25, 50, 100, and 200 µmol/L 3-BrPA for 6 h resulted in intracellular adenosine triphosphate levels of 96.98%, 88.44%, 43.3% and 27.56% relative to the control level respectively. CONCLUSION: MCT1 can enhance the sensitivity of breast cancer cells to 3-BrPA possibly by transporting 3-BrPA into cells to inhibit cell glycolysis.
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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]
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Nova |
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]
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 pro... [more]
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.
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Nova |
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]
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 a... [more]
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.
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Nova |
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]
Radiotherapy and adjuvant cisplatin chemotherapy are the mainstream approaches in the treatment of nasopharyngeal carcinoma (NPC). These have been shown to effectively improve the... [more]
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.
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Nova |
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]
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 th... [more]
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.
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Nova |
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.
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Nova |
2016 |
Jin L, Chen J, Liu XY, Jiang CC, Zhang XD, 'The double life of RIPK1.', Mol Cell Oncol, 3 e1035690 (2016) [C1]
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Nova |
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]
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Nova |
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.
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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.
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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)
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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]
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 ... [more]
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.
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Nova |
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.
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Nova |
2015 |
Tay KH, Liu X, Chi M, Jin L, Jiang CC, Guo ST, et al., 'Involvement of vacuolar H
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 appr... [more]
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.
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Nova |
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]
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Nova |
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]
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Nova |
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]
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Nova |
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)
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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]
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Nova |
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]
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 patho... [more]
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.
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Nova |
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]
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Nova |
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 BRAFV600E 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.
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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)
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 antitu... [more]
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. Interestingly, 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
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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)
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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.
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Nova |
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
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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.
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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]
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Nova |
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]
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 t... [more]
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.
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Nova |
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]
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Nova |
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]
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Nova |
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.
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Nova |
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]
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Nova |
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]
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Nova |
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.
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Nova |
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)
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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]
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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-1HCQ 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.
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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.
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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) |
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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) |
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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) |
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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.
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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) |
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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]
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Nova |
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.
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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.
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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]
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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 (Retracted article. See vol. 48, pg. 188, 2021)', INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 31 1234-1242 (2013) [C1]
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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]
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2013 |
Zhao SR, Duan HF, Zhang P, Liu H, Jiang CC, Jiang ZW, '[2-DG enhances TRAIL-induced apoptosis of leukemia HL-60 cells]', Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology, 21 351-355 (2013)
This study was purposed to investigate the effects of 2-deoxy-D-glucose (2-DG) on sensitizing HL-60 cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induce... [more]
This study was purposed to investigate the effects of 2-deoxy-D-glucose (2-DG) on sensitizing HL-60 cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis and its possible mechanism. The proliferative inhibition of HL-60 cells treated with different concentrations of 2-DG and TRAIL was measured by MTT assay. The cells were treated with 2-DG, TRAIL, and 2-DG combined with TRAIL at the concentration < IC50 value, i.e. 10 mmol/L for 2-DG and 100 ng/ml for TRAIL. Apoptosis was analyzed by flow cytometry with PI staining; the expression of RIP1, GRP78, and PARP was analyzed by Western blot; the activity of caspase-3 was detected by special detection kit. The results showed that the combined treatment of HL-60 cells for 48 h induced an apoptotic rate of (45.1 ± 4.3)%, which was significantly higher than that of treated with 2-DG or TRAIL alone; at the same time, the combined treatment potentiated the expression of GRP78 and caspase-3 activity, and down-regulated the expression of RIP1. It is concluded that 2-DG can sensitize HL-60 cells to TRAIL-induced apoptosis, which may be correlated with excessive endoplasmic reticulum stress response, down-regulation of RIP1, and increase of caspase-3 activity.
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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]
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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]
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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]
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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]
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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; IC50 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.
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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.
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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.
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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]
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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]
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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]
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Nova |
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.
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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]
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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.
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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]
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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]
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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]
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Nova |
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) |
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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]
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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]
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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]
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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]
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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]
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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]
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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) |
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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]
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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]
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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]
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Nova |
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]
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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]
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2007 |
Hersey P, Zhang XD, Jiang C, 'Endoplasmic stress (ER) in melanoma cells.', Arch Dermatol Res., 289-299 (2007) |
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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]
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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]
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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]
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