Rugang Zhang, Ph.D.

Rugang Zhang, Ph.D.

  • Deputy Director, The Wistar Institute Cancer Center
  • Professor and Co-Program Leader, Gene Expression and Regulation Program
  • 215-495-6840, Office

The Zhang laboratory studies the mechanisms that underlie how normal mammalian cells age and how tumor cells evade the process and become transformed. In particular, his laboratory is interested in how alterations in epigenetics—heritable changes that affects gene expression without changes in the underlying DNA sequence—lead to the evasion of the aging process during tumor development. Understanding these mechanisms could lead to novel strategies for developing cancer therapeutics by forcing tumor cells into the aging process. His laboratory primarily focuses on ovarian cancer, which ranks first as the cause of death for gynecological cancers in the developed world.

Born and educated in China, Zhang received his Ph.D. degree from the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences in 2002. He did his post-doctoral training at the Institute for Cancer Research, Fox Chase Cancer Center, where he became an Assistant Professor in 2008. Zhang joined The Wistar Institute as an Associate Professor in 2012. He is also an adjunct Associate Professor at University of Pennsylvania.

Selected Publications

1. Stephen TL, Payne KK, Chaurio RA, Allegrezza MJ, Zhu H, Perez-Sanz J, Perales-Puchalt A, Nguyen JM, Vava-Ailor AE, Eruslanov EB, Borowsky ME, Zhang R, Laufer TM, Conejo-Garcia JR. SATB1 expression governs epigentic repression of PD-1 in tumor-activated T cells. Immunity. 46: 51-64, 2017. PMCID: in process.

2. Svoronos N, Perales-Puchalt A, Allegrezza MJ, Rutkowski MR, Payne KK, Tesone AJ, Nguyen JM, Curiel TJ, Cadungog MG, Singhal S, Eruslanov EB, Zhang P, Tchou J, Zhang R, Conejo-Garcia JR. Tumor Cell-Independent Estrogen Signaling Drives Disease Progression through Mobilization of Myeloid-Derived Supressor Cells. Cancer Discovery. 7: 72-85, 2017. PMCID: PMC5222699.

3. Aird KM, Iwasaki O, Kossenkov A, Tanizawa H, Fatkhutdinov N, Bitler BG, Le L, Alicea G, Yang T, Noma K, Zhang R.  HMGB2 orchestrates the chromatin landscape of senescence-associated secretory phenotype gene loci.  Journal of Cell Biology. 215: 325-334, 2016. PMCID: PMC5100296.

4. Zhu H, Bengsch F, Svoronons N, Rutkowski MR, Bitler BG, Allegrezza MJ, Yokoyama Y, Bradner JE, Conejo-Garcia JR, Zhang R.  BET bromodomain inhibiton promotes anti-tumor immunity by suppressing PD-L1 expression.  Cell Reports. 16:2829-2837, 2016. PMCID: PMC5177024.

5. Yokoyama Y, Zhu H, Lee JH, Kossenkov AV, Wu S, Wickramasinghe JM, Yin X, Palozola KC, Gardini A, Showe LC, Zaret KS, Liu Q, Speicher D, Conejo-Garcia JR, Bradner JE, Zhang Z, Sood AK, Ordog T, Bitler BG, Zhang R.  BET inhibitors suppress ALDH activity by targeting ALDH1A1 super-enhancer in ovarian cancer. Cancer Research. 76:6320-6330, 2016. PMCID: in progress.

6. Aird KM, Worth AJ, Snyder NW, Lee JV, Sivanand S, Liu Q, Blair IA, Wellen KE, Zhang R. ATM couples replication stress and metabolic reprogramming during cellular senescence.  2015.  Cell Reports. 11:893-901. PMC4431925.

7. Biter BG, Aird KM, Garipov A, Li H, Amatangelo M, Kossenkov AV, Schultz DC, Liu Q, Shih IM, Conejo-Garcia JR, Speicher DW, Zhang R. Synthetic lethality by targeting EZH2 methyltransferase activity in ARID1A-mutated cancers. Nature Medicine. 21:231-238, 2015. PMC4352133.

8. Zhu H, Ren S, Bitler BG, Aird KM, Tu Z, Skordalakes E, Zhu Y, Yan J, Sun Y, Zhang R. SPOP E3 Ubiquitin Ligase Adaptor Promotes Cellular Senescence by Degrading the SENP7 deSUMOylase.  2015.  Cell Reports. 13:1183-1193. PMC4644472.

9. Aird KM, Zhang G, Li H, Tu Z, Bitler BG, Garipov A, Wu H, Wei Z, Wagner SN, Herlyn M, Zhang R. Suppression of nucleotide metabolism underlies the establishment and maintenance of oncogene-induced senescence. Cell Reports. 3: 1252-1265, 2013. PMC3840499.

10. Tu Z, Nicodemus J, Beehary N, Xia B, Yen T, Zhang R. Oncogenic Ras regulates BRIP1 expression to induce dissociation of BRCA1 from chromatin, inhibit DNA repair, and promote senescence. Developmental Cell. 21: 1077-1091, 2011PMC3241855.