Dr Lei Jin

Dr Lei Jin

Research Fellow

School of Medicine and Public Health

Career Summary

Biography

As a researcher at early career stage, Dr Lei Jin has a relatively long history (7 years) in translational melanoma research.  He is currently leading the cell death group of melanoma research laboratory that comprises 2 visiting academics, 4 PhD students and 1 research assistant.  In the past 5 years, he has published 24 research articles in high impact journals including Nature Communications, PNAS, Cancer Research, Autophagy, Oncogene, Cell Death and Differentiation and Stem cells.  
Since Dr Jin joined in HMRI in 2013, as the Chief Investigator A, he has attracted an National Health and Medical Research Council (NHMRC) project grant, 2 Hunter Medical Research Institute project grants and a Faculty of Health and Medicine Strategic Pilot Grant. In addition, as a Chief Investigator, Dr Jin has received a number of competitive grants from other sources including the National Natural Science Fund of China and Faculty of Health and Medicine. Particularly, he was awarded Hunter Translational Cancer Research Unit Fellowship in 2013 and a highly competitive Cancer Institute NSW Early Career Fellowship in 2014. 
Dr Jin has served as a reviewer to assess grant applications for national and international funding bodies including NHMRC and the National Natural Science Fund of China. He also has been invited to review manuscripts for a number of journals including Cancer Research, Oncogene, Neoplasia, Molecular Cancer Therapeutics, Molecular Cancer Research, and PLOS One.  Dr Jin actively participates in activities of academic organizations, including American Association for Cancer Research (AACR), the Australia and New Zealand Melanoma Trials Group, Melanoma Institute Australia, Melanoma Tumour Group of the Hunter New England Area Health, and Hunter Medical Research Institute.
Dr Jin has ongoing collaborations with a large number of researchers locally, nationally, and internationally.  In particular, he has established productive collaborations with researchers in China, including Professor Zhiyin Song of Wuhan University and Professors Mian Wu and Yide Mei of the University of Science and Technology of China.  These collaborations not only enable him to attract international students and visiting academics to the laboratory, but also make possible for him as a collaborator to apply for funding from various sources in China. He also provides a consultancy service to other researchers in Newcastle on molecular biology and biochemistry techniques on a daily basis.
Dr Jin pioneered studies on “overcoming resistance mechanisms of melanoma cells to chemotherapy and targeted therapy”, which has provided a number of insights into resistance mechanisms of melanoma to cell death induced by various treatments. He was also among the first to show that p53 (a common tumour suppressor gene) played a pro-survival role in melanoma cells upon endoplasmic reticular stress (a type of cellular 'stress' that occurs in many types of cancer). More recently, Dr Jin has become a leading figure in investigation of the roles of microRNAs and Receptor-Interacting Protein Kinases in regulation of melanoma cell survival and proliferation.
Dr Jin is actively engaged in communications with the general public, in particular, melanoma patients and their friends and relatives.  He regularly presents the work in lay language to various community groups, such as members of Newcastle Melanoma Foundation and Melanoma Institute Australia. He also writes newsletters for these organizations.

Qualifications

  • Doctor of Natural Science, University of Science and Technology of China

Professional Experience

UON Appointment

Title Organisation / Department
Research Fellow University of Newcastle
School of Medicine and Public Health
Australia
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Publications

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


Journal article (23 outputs)

Year Citation Altmetrics Link
2016 Chen J, Jiang CC, Jin L, Zhang XD, 'Regulation of PD-L1: a novel role of pro-survival signalling in cancer.', Ann Oncol, 27 409-416 (2016)
DOI 10.1093/annonc/mdv615
Co-authors Chenchen Jiang, Xu Zhang
2015 Tay KH, Liu X, Chi M, Jin L, Jiang CC, Guo ST, et al., 'Involvement of vacuolar H+-ATPase in killing of human melanoma cells by the sphingosine kinase analogue FTY720', Pigment Cell and Melanoma Research, 28 171-183 (2015) [C1]

© 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. Howe... [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 Web of Science - 1
Co-authors Chenchen Jiang, Xu Zhang, Nikki Verrills
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
Co-authors Chenchen Jiang, Xu Zhang, Hubert Hondermarck
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 - 1Web of Science - 1
Co-authors Xu Zhang, Chenchen Jiang
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.

Citations Scopus - 4Web of Science - 3
Co-authors Xu Zhang, Chenchen Jiang
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 - 19Web of Science - 12
Co-authors Chenchen Jiang, 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 - 14Web of Science - 11
Co-authors Chenchen Jiang, 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 - 5Web of Science - 5
Co-authors Chenchen Jiang, Xu Zhang
2014 Dong L, Jin L, Tseng H-Y, Wang CY, Wilmott JS, Yosufi B, et al., 'Oncogenic suppression of PHLPP1 in human melanoma', ONCOGENE, 33 4756-4766 (2014) [C1]
DOI 10.1038/onc.2013.420
Citations Scopus - 5Web of Science - 2
Co-authors Chenchen Jiang, 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 - 10Web of Science - 6
Co-authors Xu Zhang, Chenchen Jiang
2013 Ye Y, Li Q, Hu WL, Tseng HY, Jin L, Zhang XD, et al., 'Loss of PI(4,5)P2 5-phosphatase A contributes to resistance of human melanoma cells to RAF/MEK inhibitors', Translational Oncology, 6 470-481 (2013) [C1]

Past studies have shown that the inositol polyphosphate 5-phosphatase, phosphatidylinositol 4,5-bisphosphate 5-phosphatase (PIB5PA), is commonly downregulated or lost in melanomas... [more]

Past studies have shown that the inositol polyphosphate 5-phosphatase, phosphatidylinositol 4,5-bisphosphate 5-phosphatase (PIB5PA), is commonly downregulated or lost in melanomas, which contributes to elevated activation of phosphatidylinositol 3-kinase (PI3K)/Akt in melanoma cells. In this report, we provide evidence that PIB5PA deficiency plays a role in resistance of melanoma cells to RAF/mitogen-activated protein kinase kinase (MEK) inhibitors. Ectopic expression of PIB5PA enhanced apoptosis induced by the RAF inhibitor PLX4720 in BRAFV600E and by the MEK inhibitor U0126 in both BRAFV600E and wild-type BRAF melanoma cells. This was due to inhibition of PI3K/Akt, as co-introduction of an active form of Akt (myr-Akt) abolished the effect of over-expression of PIB5PA on apoptosis induced by PLX4720 or U0126. While overexpression of PIB5PA triggered activation of Bad and down-regulation of Mcl-1, knockdown of Bad or overexpression of Mcl-1 recapitulated, at least in part, the effect of myr-Akt, suggesting that regulation of Bad and Mcl-1 is involved in PIB5PA-mediated sen-sitization of melanoma cells to the inhibitors. The role of PIB5PA deficiency in BRAF inhibitor resistance was confirmed by knockdown of PIB5PA, which led to increased growth of BRAFV600E melanoma cells selected for resistance to PLX4720. Consistent with its role in vitro, overexpression of PIB5PA and the MEK inhibitor selumetinib cooperatively inhibited melanoma tumor growth in a xenograft model. Taken together, these results identify loss of PIB5PA as a novel resistance mechanism of melanoma to RAF/MEK inhibitors and suggest that restoration of PIB5PA may be a useful strategy to improve the therapeutic efficacy of the inhibitors in the treatment of melanoma. © 2013 Neoplasia Press, Inc. All rights reserved.

DOI 10.1593/tlo.13277
Citations Scopus - 5Web of Science - 4
Co-authors Xu Zhang
2013 Han C, Jin L, Mei Y, Wu M, 'Endoplasmic reticulum stress inhibits cell cycle progression via induction of p27 in melanoma cells', Cellular Signalling, 25 144-149 (2013) [C1]

The accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggers the unfolded protein response (UPR), a stress signaling pathway. The UPR coordinates the induction... [more]

The accumulation of unfolded proteins in the endoplasmic reticulum (ER) triggers the unfolded protein response (UPR), a stress signaling pathway. The UPR coordinates the induction of ER chaperones with decreased protein synthesis and growth arrest in G1 phase of the cell cycle. However, the molecular mechanism underlying UPR-induced G1 cell cycle arrest remains largely unknown. Here we report that activation of the UPR response by tunicamycin (TM), an ER stress inducer, leads to accumulation of p27 and G1 cell cycle arrest in melanoma cells. This accumulation of p27 is due to the inhibition on its polyubiquitination and subsequent degradation upon TM treatment. Correlated with p27 stabilization, the levels of Skp2, an E3 ligase for p27, are decreased in response to TM treatment. More importantly, knockdown of p27 greatly reduces TM-induced G1 cell cycle arrest. Taken together, these data implicate p27 as a critical mediator of ER stress-induced growth arrest. © 2012 Elsevier Inc.

DOI 10.1016/j.cellsig.2012.09.023
Citations Scopus - 13
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 - 72Web of Science - 44
Co-authors Xu Zhang, Rick Thorne, Chenchen Jiang
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 - 25Web of Science - 19
Co-authors Rick Thorne, Xu Zhang, Chenchen Jiang
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 - 15Web of Science - 10
Co-authors Chenchen Jiang, 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 - 9Web of Science - 8
Co-authors Xu Zhang, Chenchen Jiang
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 - 6Web of Science - 4
Co-authors Chenchen Jiang, Xu Zhang
2012 Wang J, He Q, Han C, Gu H, Jin L, Li Q, et al., 'p53-facilitated mir-199a-3p regulates somatic cell reprogramming', Stem Cells, 30 1405-1413 (2012) [C1]

Somatic cells can be reprogrammed to induced pluripotent stem cells (iPSCs) by ectopic expression of defined transcriptional factors. The efficiency of this process, however, is e... [more]

Somatic cells can be reprogrammed to induced pluripotent stem cells (iPSCs) by ectopic expression of defined transcriptional factors. The efficiency of this process, however, is extremely low. Although inactivation of p53 has been recently shown to greatly enhance reprogramming efficiency, the underlying molecular mechanisms still remain largely unknown. Here, we report that miR-199a-3p is upregulated by p53 at the post-transcriptional level. Induction of miR-199a-3p significantly decreases reprogramming efficiency, whereas miR-199a-3p inhibition greatly enhances it. Mechanistically, miR-199a-3p overexpression inhibits cell proliferation by imposing G1 cell cycle arrest. Conversely, miR-199a-3p inhibition results in a pronounced increase in cell proliferation. Furthermore, the enhancement in reprogramming of p53 knockdown cells is almost completely reversed with replacement of miR-199a-3p. Also, miR-199a-3p inhibition partially rescues iPS generation impaired by p53. These findings suggest miR-199a-3p as a novel p53 target that negatively regulates somatic cell reprogramming. © AlphaMed Press.

DOI 10.1002/stem.1121
Citations Scopus - 35
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 e337 (2012) [C1]
Citations Scopus - 18Web of Science - 16
Co-authors Rick Thorne, Chenchen Jiang, Nikki Verrills, Xu Zhang
2011 Qin S, Jin L, Zhang J, Liu L, Ji P, Wu M, et al., 'Recognition of unmodified histone H3 by the first PHD finger of bromodomain-PHD finger protein 2 provides insights into the regulation of histone acetyltransferases monocytic leukemic zinc-finger protein (MOZ) and MOZ-related factor (MORF)', Journal of Biological Chemistry, 286 36944-36955 (2011) [C1]

MOZ (monocytic leukemic zinc-finger protein) and MORF (MOZ-related factor) are histone acetyltransferases important for HOX gene expression as well as embryo and postnatal develop... [more]

MOZ (monocytic leukemic zinc-finger protein) and MORF (MOZ-related factor) are histone acetyltransferases important for HOX gene expression as well as embryo and postnatal development. They form complexes with other regulatory subunits through the scaffold proteins BRPF1/2/3 (bromodomain- PHD (plant homeodomain) finger proteins 1, 2, or 3). BRPF proteins have multiple domains, including two PHD fingers, for potential interactions with histones. Here we show that the first PHD finger of BRPF2 specifically recognizes the N-terminal tail of unmodified histone H3 (unH3) and report the solution structures of this PHD finger both free and in complex with the unH3 peptide. Structural analysis revealed that the unH3 peptide forms a third antiparallel ß-strand that pairs with the PHD1 two-stranded antiparallel ß-sheet. The binding specificity was determined primarily through the recognition of arginine 2 and lysine 4 of the unH3 by conserved aspartic acids of PHD1 and of threonine 6 of the unH3 by a conserved asparagine. Isothermal titration calorimetry and NMR assays showed that post-translational modifications such as H3R2me2as, H3T3ph, H3K4me, H3K4ac, and H3T6ph antagonized the interaction between histone H3 and PHD1. Furthermore, histone binding by PHD1 was important for BRPF2 to localize to the HOXA9 locus in vivo. PHD1 is highly conserved in yeast NuA3 and other histone acetyltransferase complexes, so the results reported here also shed light on the function and regulation of these complexes. © 2011 by The American Society for Biochemistry and Molecular Biology, Inc.

DOI 10.1074/jbc.M111.244400
Citations Scopus - 27
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]
Citations Scopus - 74Web of Science - 64
Co-authors Chenchen Jiang, Xu Zhang, Rick Thorne
2010 Miao L, Song Z, Jin L, Zhu YM, Wen LP, Wu M, 'ARF antagonizes the ability of Miz-1 to inhibit p53-mediated transactivation', Oncogene, 29 711-722 (2010) [C1]

Although Myc-interacting zinc-finger protein-1 (Miz-1) is known to be a poxvirus and zinc-finger (POZ) transcription factor required for Myc transcriptional repression, additional... [more]

Although Myc-interacting zinc-finger protein-1 (Miz-1) is known to be a poxvirus and zinc-finger (POZ) transcription factor required for Myc transcriptional repression, additional regulatory function of Miz-1 is less well understood. Using a yeast two-hybrid screen, we identified human alternate reading frame (ARF) protein as a novel interaction partner of Miz-1. The zinc-finger domain of Miz-1 is involved in its binding to ARF. In addition, we found that Miz-1 was able to interact with p53 through its DNA-binding domain, thus to diminish the binding of p53 to its target promoter and inhibit p53-mediated gene transcription. Interestingly, the Miz-1-regulated p53 transcriptional suppression does not require the presence of ARF or Mdm2. Importantly, ARF and p53 were found to competitively bind to Miz-1 in regulating p53-mediated transcription, and this conclusion was verified by both in vitro binding assay and competitive chromatin immunoprecipitation assay using a bona fide p53 endogenous Bax and Puma promoters. Thus, our study reveals that Miz-1 acts as a p53 suppressor by interfering with p53 DNA-binding ability, and ARF is able to counteract the suppression of Miz-1 on p53 by direct binding to Miz-1, suggesting that Miz-1 is a novel mediator in the ARF-p53 pathway. © 2010 Macmillan Publishers Limited All rights reserved.

DOI 10.1038/onc.2009.372
Citations Scopus - 12
2006 Zhu D-E, Höti N, Song Z, Jin L, Wu Z, Wu Q, Wu M, 'Suppression of tumor growth using a recombinant adenoviral vector carrying the dominant-negative mutant gene Survivin-D53A in a nude mice model', Cancer Gene Therapy, 13 762-770 (2006)
DOI 10.1038/sj.cgt.7700952
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Conference (14 outputs)

Year Citation Altmetrics Link
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 Chenchen Jiang, Hubert Hondermarck, Xu Zhang
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 (2015) [E3]
Co-authors Chenchen Jiang, Xu Zhang
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, Chenchen Jiang
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 Chenchen Jiang, Xu Zhang
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 (2014) [E3]
Co-authors Xu Zhang, Chenchen Jiang
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 (2014) [E3]
Co-authors Xu Zhang, Chenchen Jiang
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 (2014) [E3]
Co-authors Xu Zhang, Chenchen Jiang
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. (2014) [E3]
Co-authors Xu Zhang, Chenchen Jiang
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 Chenchen Jiang, Xu Zhang
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, Chenchen Jiang
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 Xu Zhang, Rodney Scott, Rick Thorne, Chenchen Jiang, Stephen Ackland
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, Chenchen Jiang
2013 Jin L, Li D, Wang CY, Tseng H-Y, Wilmott JS, Yosufi B, et al., 'PHLPP1 Deactivates Akt and has a Tumour Suppressive Role in Human Melanoma', JOURNAL DER DEUTSCHEN DERMATOLOGISCHEN GESELLSCHAFT (2013) [E3]
Co-authors Xu Zhang
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 Xu Zhang, Chenchen Jiang
Show 11 more conferences
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Grants and Funding

Summary

Number of grants 8
Total funding $1,303,943

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


20161 grants / $401,786

Alpha-actinin-4 as an oncogenic driver and therapeutic target in melanoma$401,786

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

Funding body NHMRC (National Health & Medical Research Council)
Project Team Doctor Lei Jin
Scheme Project Grant
Role Lead
Funding Start 2016
Funding Finish 2018
GNo G1500133
Type Of Funding Aust Competitive - Commonwealth
Category 1CS
UON Y

20154 grants / $89,698

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

A Novel Approach to Destruct Melanoma$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Lei Jin, Professor Xu Dong Zhang
Scheme Project Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1501379
Type Of Funding Grant - Aust Non Government
Category 3AFG
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
Scheme Strategic Research Pilot Grant
Role Lead
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
Project Team
Scheme Strategic Research Pilot Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo
Type Of Funding Internal
Category INTE
UON N

20142 grants / $612,459

RIPK1 as a novel therapeutic target in melanoma$592,459

Funding body: Cancer Institute NSW

Funding body Cancer Institute NSW
Project Team Doctor Lei Jin
Scheme Early Career Fellowship
Role Lead
Funding Start 2014
Funding Finish 2016
GNo G1300920
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

RIPK1 as a novel therapeutic target in melanoma$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Lei Jin, Professor Xu Dong Zhang
Scheme Project Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1301258
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20131 grants / $200,000

Hunter Translational Cancer Research Unit Post-doctoral Fellowship$200,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team
Scheme Post-doctoral Fellowship
Role Lead
Funding Start 2013
Funding Finish 2014
GNo
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON N
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Research Supervision

Number of supervisions

Completed0
Current5

Total current UON EFTSL

PhD2.25

Current Supervision

Commenced Level of Study Research Title / Program / Supervisor Type
2015 PhD Identification and Characterisation of Apoptosis-Regulating Long Noncoding RNAs in Melanoma
PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor
2015 PhD To Look at Long Non-Coding RNAs in Melanoma
PhD (Medical Biochemistry), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor
2015 PhD Novel Signalling Pathways in Food Allergy and Eosinophilic Oesophagitis
PhD (Immunology & Microbiol), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor
2015 PhD Functional Consequences of Up-Regulation of ACTN4 in Melanoma
PhD (Medicine), Faculty of Health and Medicine, The University of Newcastle
Co-Supervisor
2014 PhD Targeting Human Mut T Homolog1 in Melanoma
PhD (Medical Biochemistry), 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 26
China 24
United Kingdom 1
United States 1
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News

NHMRC

NHMRC funding success 2016

November 13, 2015

Dr Lei Jin has been awarded more than $401,000 in NHMRC Project Grant funding commencing in 2016 for his research project Alpha-actinin-4 as an oncogenic driver and therapeutic target in melanoma.

Matt Dun

$1.5m to Newcastle researchers to unlock cancer secrets

February 21, 2014

Three University of Newcastle cancer researchers have been recognised with Cancer Institute NSW Early Career Fellowships, totalling more than $1.5 million.

Dr Lei Jin

Position

Research Fellow
Melanoma Research Labratory
School of Medicine and Public Health
Faculty of Health and Medicine

Contact Details

Email lei.jin@newcastle.edu.au
Phone (02) 4921 8689

Office

Room LS3-38
Building Life Science Building
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