Profile

Dr. Junxia Min currently serves as a professorat Institute of Translational Medicine, Zhejiang University, Hangzhou, China. Her research interest is mainly focused on three areas: 1. to explore cancer’s novel therapeutics, including molecular targeted therapy and immunotherapy, for gastrointestinal cancer; 2. to elucidate molecular mechanisms of resistance to targeted cancer therapeutics; 3.to further refine our previously established causal network models for realizably predicting drug sensitivity and defining driving pathways in Chinese-prevalent cancer types.Dr. Min earned her Ph.D. from University of Missouri-Columbia in 2006. During her 4 year-Ph.D. training period, she published 7 peer-reviewed research articles. Her key finding was discovered and defined the important roles of sphingo lipid metabolic pathway in resistance to platinum-based anticancer drugs. Her findings opened new avenue for targeting sphingo lipid metabolic pathway in cancer therapeutics. In 2006, Dr. Min went to Harvard Medical School, where she spent over 4.5 years for her postdoctoral training at the Department of Medicine, Brigham and Women’s Hospital. Her major scientific achievement was identification and functional characterization of EZH2/DAB2IP as oncogene-tumor suppressor cascade in promoting prostate cancer tumorigenesis and progression. The finding was highlighted as the breakthrough of year 2010 in prostate cancer research and on The Wall Street Journalhttp://online.wsj.com/news/articles/SB10001424052748703279704575334982806405218.Since 2010, Dr. Min joined Novartis as a research investigator/postdoc mentor at Cambridge, U.S.A. Using integrative meta-analysis in conjunction with functional screens, Dr. Min's group focused on target identification and validation. For tumor suppressor genes, such as p53, Min group was strived to identify critical synthetic lethal nodes by employing large-scale RNAi screening.In addition, Dr. Minisalso interested in understanding molecular mechanisms of resistance in response to targeted therapies.Research InterestNovel Target Discovery: Molecularly targeted cancer therapies are designed to specifically block the driving ‘oncogenes’ that sustain tumorigenesis and tumor progression while sparing normal cells. Gleevec, which targets BCR-ABL in CML, was one of the first demonstrations of this new paradigm of cancer treatment, and has clinically been proven to be more effective and less toxic than chemotherapies. To discover novel cancer therapeutic targets, our laboratory is focusing on applying integrative genomic and functional approaches. For tumor suppressor genes, such as p53, we aim to discover critical synthetic lethal nodes by employing large-scale RNAi screening. Synthetic lethal nodes are defined as genes that only become essential in the context of another mutation. Thus, it is expected that targeting synthetic lethal genes of key cancer pathways would provide wider therapeutic windows compared to cytotoxic chemotherapeutics.Cancer Immunotherapy: It refers a strategy that harnesses the body's immune system to combat tumors. With remarkable durable-response, cancer immunotherapy was selected as the breakthrough of the Year for 2013. The recent successful story of immune-checkpoint blockade ipilimumab (Yervoy) for melanoma, and novel chimeric T cell therapy-CART19 for CLL and ALL patients, have raised hope that immunotherapy may provide oncologists new options for treatment in the future. By using what we have learned about the immune system, we aim to explore effective immunotherapeutic target for Chinese-prevalent cancer types.Molecular Mechanisms of Resistance: In addition, we are interested in understanding mechanisms of resistance in response to cancer therapies, in particular mechanisms that circumvent response to targeted therapies. We are using primary xenograft models (PTX) to study the causal genes or pathways that account for the resistance to targeted therapies. Cancer Network Metadata Analysis: Another area of research interest is to discover novel therapeutic approaches for cancers that currently lack of targeted therapy, such as triple-negative breast cancer (TNBC). Using network analysis in couple with genomic and epigenetic profiling data mining, we aim to define driving pathways in molecularly defined subtypes of Asian prevalent cancer.Selected Publications （*Corresponding author）：1. Yi Zeng#, Chao Nie#, Junxia Min#, Xiaomin Liu#, Mengmeng Li, Huashuai Chen, Hanshi Xu, Mingbang Wang, Ting Ni, Yang Li, Han Yan, JinPei Zhang, Chun Song, Li Qing Chi, Han Ming Wang, Jie Dong, Gu-Yan Zheng, Li Lin, Feng Qian, Yanwei Qi,Xiao Liu, Hongzhi Cao, Yinghao Wang, Lijuan Zhang, Zhaochun Li, Yufeng Zhou,Yan Wang, Jiehua Lu, Jianxin Li, Ming Qi, Lars Bolund, Anatoliy Yashin,KennethC Land, Simon Gregory, Ze Yang, William Gottschalk, Wei Tao,Jian Wang, Jun Wang, Xun Xu, Harold Bae, Marianne Nygaard, Lene Christiansen, Kaare Christensen, Claudio Franceschi, MichaelW Lutz, Jun Gu, Qihua Tan,Thomas Perls, Paola Sebastiani, Joris Deelen, Eline Slagboom, Elizabeth Hauser, Huji Xu, XiaoLi Tian, Huanming Yang and JamesW Vaupel. Novel loci and pathways significantly associated with longevity. Scientific Reports. 2016 Feb 25;6:21243. 2. Zeng Y, Chen H, Ni T, Ruan R, Nie C, Liu X, Feng L, Zhang F, Lu J, Li J, Li Y, Tao W, Gregory SG, Gottschalk W, Lutz MW, Land KC, Yashin A, Tan Q, Yang Z, Bolund L, Ming Q, Yang H, Min J, Willcox DC, Willcox BJ, Gu J, Hauser E, Tian XL, Vaupel JW. Interaction Between the FOXO1A-209 Genotype and Tea Drinking Is Significantly Associated with Reduced Mortality at Advanced Ages. Rejuvenation Research. 2016 Feb 10. [Epub ahead of print]3. Fang X,Wei J,He X,An P,Wang H,Jiang L,Shao D,Liang H,Li Y,Wang F*,Min J*. Landscape of dietary factors associated with risk of gastric cancer: A systematic review and dose-response meta-analysis of prospective cohort studies. Eur J Cancer.2015 Dec;51(18):2820-32. doi: 10.1016/j.ejca.2015.09.010. 4. An P, Zhou D, Wang H, Wu Q, Guo X, Wu A, Zhang Z, Zhang D, Xu X, Mao Q, Shen X, Zhang L, Xiong Z, He L, Min J*, Liu Y* and Wang F*. Elevated serum transaminase activities were associated with increased serum levels of iron regulatory hormone hepcidin and hyperferritinemia risk. Scientific Reports, 2015 Aug 20;5:13106. doi: 10.1038/srep13106.5. Fang X, Wang H, An P, Min J, and Wang F*. Cardiomyocyte-specific deletion of ferroportin using MCK-Cre has no apparent effect on either cardiac iron homeostasis. International Journal of Cardiology, 2015 Dec 15;201:90-2. doi: 10.1016/j.ijcard.2015.07.0896. Mu M, An P, Shen X, Wu Qian, Shao D, Wang H, Zhang Y, Zhang S, Yao H, Min J*, Wang F*. The dietary flavonoid myricetin regulates iron homeostasis by suppressing hepcidin expression. Journal of Nutritional Biochemistry. 2015 doi:10.1016/j.jnutbio.2015.10.015. (* co-corresponding author）7. WANG Hong-Xiao, MIN Jun-Xia* Advances in discovering anticancer agents from plant secondary metabolites and their derivatives, Chinese Bulletin of Life Sciences, 2015, Aug, 27(8).1006-19, DOI: 10.13376/j.cbls/20151408. Zhou Q., Derti A., Ruddy D., Rakiec D., Kao I., Lira M, Gibaja V, Chan H, Yang Y, Min J, Schlabach M, Stegmeier F. A chemical genetics approach for the functional assessment of novel cancer genes. Cancer Research. 2015 May 15;75(10):1949-58. doi: 10.1158/0008-5472.CAN-14-29309. Wu Q, Wang H, An P, Tao Y, Deng J, Zhang Z, Shen Y, Min J*, Wang F*. HJV and HFE Play Distinct Roles in Regulating Hepcidin. Antioxidants & Redox Signaling.2015 May 20;22(15):1325-36. doi: 10.1089/ars.2013.5819 10. Huang T#, Lan L#, Fang X, An P, Min J, Wang F*. Promises and Challenges of Big Data Computing in Health Sciences. Big Data Research, 2015, 11. Wang Y, Lee YM, Baitsch L, Huang A, Xiang Y, Tong H, Lako A, Von T, Choi C, Lim E, Min J, Li L, Stegmeier F, Schlegel R, Eck MJ, Gray NS, Mitchison TJ, Zhao J. MELK is an oncogenic kinase essential for mitotic progression in basal-like breast cancer cells. eLife. 2014 May 20;3:e01763. doi: 10.7554/eLife.01763. 12. Jaeger S, Min J, Nigsch F, Camargo M, Hutz, J, Cornett A, Cleaver S, Buckler A, Jenkins JL. Causal Network Models for Predicting Compound Targets and Driving Pathways in Cancer. J Biomol Screen. 2014 Feb 11;19(5):791-802 (co-first author) 13. Min J, Zaslavsky A, Fedele G, McLaughlin SK, Reczek EE, De Raedt T, Guney I, Strochlic DE, Macconaill LE, Beroukhim R, Bronson RT, Ryeom S, Hahn WC, Loda M, Cichowski K. An oncogene-tumor suppressor cascade drives metastatic prostate cancer by coordinately activating Ras and nuclear factor-kappaB. Nature Medicine. 2010 Mar;16(3):286-94. doi: 10.1038/nm.2100. 14. Sridevi P, Alexander H, Laviad EL, Min J, Mesika A, Hannink M, Futerman AH, Alexander S. Stress-induced ER to Golgi translocation of ceramide synthase 1 is dependent on proteasomal processing. Experimental Cell Research. 2010 Jan 1;316(1):78-91. doi: 10.1016/j.yexcr.2009.09.027 15. Van Driessche N, Alexander H, Min J, Kuspa A, Alexander S, Shaulsky G. Global transcriptional responses to cisplatin in Dictyosteliumdiscoideum identify potential drug targets. Proc Natl Acad Sci U S A. 2007 Sep 25;104 (39):15406-11. 16. . Min J, Mesika A, Sivaguru M, Van Veldhoven PP, Alexander H, Futerman AH, Alexander S. (Dihydro)ceramide synthase 1 regulated sensitivity to cisplatin is associated with the activation of p38 mitogen-activated protein kinase and is abrogated by sphingosine kinase 1. Molecular Cancer Research. 2007 Aug;5(8):801-12 17. Min J, Sridevi P, Alexander S, Alexander H. Sensitive cell viability assay for use in drug screens and for studying the mechanism of action of drugs in Dictyosteliumdiscoideum. Biotechniques. 2006 Nov;41(5):591-5 18. Alexander S, Min J, Alexander H. Dictyosteliumdiscoideum to human cells: pharmacogenetic studies demonstrate a role for sphingolipids in chemoresistance. Biochim Biophys Acta. 2006 Mar;1760(3):301-9. 19. . Min J, Van Veldhoven PP, Zhang L, Hanigan MH, Alexander H, Alexander S. Sphingosine-1-phosphate lyase regulates sensitivity of human cells to select chemotherapy drugs in a p38-dependent manner. Molecular Cancer Research. 2005 May;3(5):287-96 20. Min J, Traynor D., Stegner A.L, Zhang L., Hanigan M.H., Alexander H., and Alexander S. Sphingosine kinase regulates the sensitivity of DictyosteliumDiscoideumcells to the anticancer drug cisplatin. Eukaryotic Cell, 2005;4:178-189 21. . Min J, Stegner A.L, Alexander H. and Alexander S. Overexpression of sphingosine-1-phosphate lyase or inhibition of sphingosine kinase in Dictyostelium discoideum results in a selective increase in sensitivity to platinum based chemotherapy drugs. Eukaryotic Cell, 2004;3:795-805