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Peng Wang

  • ASSISTANT PROFESSOR Medicine, Endocrinology, Diabetes and Bone Disease
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  • B.S., Shenyang Agricultural University

  • Ph.D., Institute of Genetics and Developmental Biology, Chinese Academy of Science

  • Postdoc, University of Pittsburgh


    Dr. Peng Wang has worked in the field of cellular proliferation and cell death for 15 years. He has studied the cellular and molecular mechanisms of programmed cell death in cancer cells induced by anticancer drugs. He has identified and separated the nuclear function of the important tumor suppressor, p53, on apoptosis induced by DNA damaging agents. He also delineated the cross-talk between the intrinsic and extrinsic death pathways through transcriptional regulation, and the cross-talk between autophagy and apoptosis through caspase-mediated Beclin-1 cleavage.  He has also contributed to understanding how microRNAs regulate cancer cell proliferation.


    In the past two years, Dr. Wang has turned his focus to pancreatic beta cell proliferation.  Using his background described above on cell death and proliferation signaling pathways, he is: 1) developing cell-based strategies for small molecular screens aimed at inducing human beta cell expansion and survival; 2) using molecular approaches to generate continuously growing human beta cell lines using lentiviral systems; and, 3) using shRNA RNA and related approaches to silence cell cycle inhibitors in human beta cells, with the goal of inducing sustained, regulatable, and safe proliferation in human beta cells.


Ming L, Wang P, Bank A, Yu J, Zhang L. PUMA Dissociates Bax and Bcl-X(L) to induce apoptosis in colon cancer cells. The Journal of biological chemistry 2006 Jun; 281(23).

Wu B, Qiu W, Wang P, Yu H, Cheng T, Zambetti GP, Zhang L, Yu J. p53 independent induction of PUMA mediates intestinal apoptosis in response to ischaemia-reperfusion. Gut 2007 May; 56(5).

Yu J, Wang P, Ming L, Wood MA, Zhang L. SMAC/Diablo mediates the proapoptotic function of PUMA by regulating PUMA-induced mitochondrial events. Oncogene 2007 Jun; 26(29).

Wang P, Yu J, Zhang L. The nuclear function of p53 is required for PUMA-mediated apoptosis induced by DNA damage. Proceedings of the National Academy of Sciences of the United States of America 2007 Mar; 104(10).

Bank A, Wang P, Du C, Yu J, Zhang L. SMAC mimetics sensitize nonsteroidal anti-inflammatory drug-induced apoptosis by promoting caspase-3-mediated cytochrome c release. Cancer research 2008 Jan; 68(1).

Wang P, Qiu W, Dudgeon C, Liu H, Huang C, Zambetti GP, Yu J, Zhang L. PUMA is directly activated by NF-kappaB and contributes to TNF-alpha-induced apoptosis. Cell death and differentiation 2009 Sep; 16(9).

Wang P, Zou F, Zhang X, Li H, Dulak A, Tomko RJ, Lazo JS, Wang Z, Zhang L, Yu J. microRNA-21 negatively regulates Cdc25A and cell cycle progression in colon cancer cells. Cancer research 2009 Oct; 69(20).

Dudgeon C, Wang P, Sun X, Peng R, Sun Q, Yu J, Zhang L. PUMA induction by FoxO3a mediates the anticancer activities of the broad-range kinase inhibitor UCN-01. Molecular cancer therapeutics 2010 Nov; 9(11).

Li H, Wang P, Sun Q, Ding WX, Yin XM, Sobol RW, Stolz DB, Yu J, Zhang L. Following cytochrome c release, autophagy is inhibited during chemotherapy-induced apoptosis by caspase 8-mediated cleavage of Beclin 1. Cancer research 2011 May; 71(10).

Li H, Wang P, Yu J, Zhang L. Cleaving Beclin 1 to suppress autophagy in chemotherapy-induced apoptosis. Autophagy 2011 Oct; 7(10).

Dudgeon C, Peng R, Wang P, Sebastiani A, Yu J, Zhang L. Inhibiting oncogenic signaling by sorafenib activates PUMA via GSK3β and NF-κB to suppress tumor cell growth. Oncogene 2012 Nov; 31(46).

Industry Relationships

Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.

Dr. Wang did not report having any of the following types of financial relationships with industry during 2015 and/or 2016: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.

Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website. Patients may wish to ask their physician about the activities they perform for companies.

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