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Zhaohui 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:

  • Zhang C., Liu J., Huang G., Zhao Y., Yue X, Wu H, Li J., Zhu J., Shen Z. Haffty BG, Hu W, Feng Z. (2016) Cullin3-    KLHL25 ubiquitin ligase targets ACLY for degradation to inhibit lipid synthesis and  tumor progression. Genes Dev. 30(17):1956-70.
  • Zhang C., Liu J., Zhao Y., Yue X., Zhu Y., Wang X., Blanco F., Wu h., Li S., Bhanot G, Haffty BG., Hu W., Feng Z. (2016) Glutaminase 2 is a novel negative regulator of Rac1 and mediates p53 function in suppressing cancer metastasis. eLIFE, 10.7554/eLife.10727. PMID: 26751560

  • Yue X., Zhao Y., Liu J., Zhang C., Yu H., Wang J., Zheng T., Liu L., Li J., Feng Z. (co-corresponding), Hu W. (2015) BAG2 promotes tumorigenesis through enhancing mutant p53 protein levels and function. eLIFE. 10.7554/eLife.08401. PMID: 26271008; PMCID: PMC4561369

  • Zhao Y, Zhang C, Yue X, Li X, Liu J, Yu H, Belyi VA, Yang Q, Feng Z (co-corresponding), Hu W. (2015)  Pontin, a new mutant p53 binding protein, promotes gain of function of mutant p53. Cell Death & Differ, 2015;22(11):1824-36. PMID: 25857266

  • Yu H., Yue X., Zhao Y., Li X., Wu L., Zhang C., Liu Z., Lin K., Xu-Monette Z., Young K., Liu J., Shen Z., Feng Z.(co-corresponding), Hu W. (2014) LIF negatively regulates tumor suppressor p53 through Stat3/ID1/MDM2 in colorectal cancers. Nature Communications, 5:5218. PMID: 25323535; PMCID: PMC4203416
  • 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, 21(11):1792-804.
  • 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)
  • Feng Z, Hu W, Tang MS.  (2004) Trans-4-hydroxy-2-nonenal inhibits nucleotide excision repair in human cells: a possible mechanism for lipid peroxidation-induced carcinogenesis. Proc Natl Acad Sci U S A, 101:8598-8602 PMID: 15187227; PMCID: PMC423240

Complete List of Published Work in MyBibliography:


PostDoc positions are available