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FengZhaohui Feng, Ph.D.

Associate Professor
Division of Radiation Cancer Biology
Tel: 732-235-8814




    • M.D. Zhejiang University School of Medicine, Hangzhou, China
    • Ph.D. Zhejiang University School of Medicine, Hangzhou, China
    • Postdoc training: New York University School of Medicine and Cancer Institute of New Jersey/UMDNJ

Research Interests:

The tumor suppressor p53 plays a critical role in maintaining genomic stability and tumor prevention. p53 is the most frequently-mutated gene in human tumors; over 50% of all tumors harbor mutations in the p53 gene, and over 80% of tumors have a dysfunctional p53 signaling pathway. As a transcription factor, p53 responds to a wide variety of stress signals. Once activated, p53 selectively transcribes a set of target genes to initiate various cellular responses, including cell cycle arrest, apoptosis, or senescence, to exert its function in tumor suppression.

We are interested in the following research themes: 1) The role of p53 in regulating cellular metabolism and how this contributes to tumor suppression. Metabolic changes have been suggested to be a hallmark of tumor cells, and have been recently identified as a key contributor to malignant progression. We are studying how p53 maintains the hemostasis of metabolism through its regulation of glucose metabolism, lipid metabolism, mitochondrial integrity, and anti-oxidant defense, and furthermore, how these functions of p53 contribute to tumor suppression. 2) The regulation of p53 in cells. To ensure the proper levels and functions of p53 in tumor suppression, p53 is tightly regulated by many different regulators and mechanisms in cells. We are interested in identifying new regulators for p53 and its signaling pathways, such as E3 ubiquitin ligases and microRNAs that regulate p53 and its negative regulator MDM2. 3) Many tumor-associated mutant p53 proteins, particularly “tumor hotspot mutants”, not only lose tumor suppressive functions of wild-type p53, but also gain new activities in promoting tumorigenesis, which is defined as mutant p53 gain-of-function. We are interested in studying the mechanisms underlying the mutant p53 gain-of-function in tumorigenesis.


Selected Peer-Reviewed Publications for the Recent 5 Years:

    • Liu J, Zhang C, Wang X, ly P, Xu-Monette Z, Belyi V, Young KH, Hu W, Feng Z. E3 ubiquitin ligase TRIM32 negatively regulates tumor suppressor p53 to promote tumorigenesis. Cell Death & Differ, in press (2014).
    • Liu J, Zhang C, Lin M, Zhu W, Liang Y, Hong X, Zhao Y, Young KH, Hu W, Feng Z. Glutaminase 2 negatively regulates the PI3K/AKT signaling and shows tumor suppression activity in human hepatocellular carcinoma. Oncotarget, 5 (9), 2635 (2014).
    • Zhang C, Liu L, Liang YJ, Rui W, Lin M, Hong X, Liu L, Levine AJ, Hu W, Feng Z. Tumor-Associated Mutant p53 Drives the Warburg Effect. Nature Communications. 4:2935 doi: 10.1038/ncomms3935 (2013).
    • Zheng T, Wang J, Zhao Y, Zhang C, Lin M, Wang X, Yu H, Liu L, Feng Z (co-corresponding), Hu W. Spliced MDM2 isoforms promote mutant p53 accumulation and gain-of-function in tumorigenesis. Nature Communications. 4:2996 doi: 10.1038/ncomms3996. (2013).
    • Feng Z, Liu L, Zhang C, Zheng T, Wang J, Lin M, Wang X, Levine AJ, Hu W. Chronic restraint stress attenuates p53 function and promotes tumorigenesis. Proc Natl Acad Sci U S A. 109(18):7013-8 (2012)
    • Zhang C. Wu R. Lin M. Wang X. Levine AJ., Hu W. Feng Z. Parkin, a novel p53 target gene, mediates the function of p53 in regulating glucose metabolism and the Warburg effect. Proc Natl Acad Sci USA., 108(39):16259-64. (2011)
    • Hu W, Chang S. Chan, Rui Wu, Zhang Z, Sun Y, Song J, Levine AJ, Feng Z. Negative Regulation of Tumor Suppressor p53 by microRNA miR-504. Mol. Cell, 38, 689–699. (2010)
    • Hu W. Zhang C., Wu R., Sun Y. Levine A.J. Feng Z. GLS2, a novel p53 target gene, regulates energy metabolism and antioxidant function. Proc Natl Acad Sci USA., 107(16):7455-60. (2010)
    • Hu W., Feng Z* (co-first author), Teresky AK., Levine AJ. p53 regulates maternal reproduction through LIF. Nature; 450 (7170): 721-724.
    • Feng Z, Hu W, Yu H, Tang MS. Acrolein is a major cigarette-related lung cancer agent: preferential binding at p53 mutational hotspots and inhibition of DNA repair Proc Natl Acad Sci U S A, 103:15404-15409.(2006)
    • Feng Z, Zhang H, Levine AJ, Jin S. The coordinate regulation of the p53 and mTOR pathways in cells. Proc Natl Acad Sci U S A, 102:8204-8209. (2005)


    PostDoc positions are available