Our Science

Rugang Zhang, Ph.D.

Rugang Zhang, Ph.D.

  • 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. 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 Epigenetically Promotes Cellular Senescence by Degrading the SENP7 deSUMOylase. Cell Reports 13(6):1183-93, 2015.

2. Bitler BG, Garipov A, Amatangelo M, Kossenkov A, Schultz DC, Shih IM, Conejo-Garcia JR, Speicher DW, Zhang R. Synthetic lethality by targeting EZH2 methyltransferase activity in ARID1A-mutated cancers. Nature Medicine 21(3): 231-238, 2015.

3. Zhao B, Zhang WD, Lu YQ, Cun YX, Li CH, Guo K, Nie WH, Li L, Zhang R, Zheng PESC-specific protein Filia is a master regulator of DNA damage response and safeguards genomic stability of mouse ESCs. Cell Stem Cell 16(6): 684-98, 2015.

4. Rutkowski MR, Stephen TL, Svoronos N, Allegrezza MJ, Perales-Puchalt A, Tesone AJ, Escovar-Fadul X, Nguyen JM, Cadungog MG, Zhang R, Salatino M, Rabinovich GA, Tchou J, Conejo-Garcia JR. Microbially driven TLR-dependent signalling governs distal malignant progression through tumor-promoting inflammation. Cancer Cell 27: 27-40, 2015.

5 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. Cell Reports 11(6): 893-901, 2015.

6. 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.

7. Tu Z, Zhuang X, Yao YG, Zhang R.BRG1 is required for formation of senescence-associated heterochromatin foci (SAHF) induced by oncogenic RAS or BRCA1 loss. Molecular and Cellular Biology 33: 1819-1829, 2013.

8. Tu, Z., Aird, K. M., Bitler, B. G., Nicodemus, J. P., Beeharry, N., Xia, B., Yen, T. J., Zhang, R.Oncogenic RAS regulates BRIP1 expression to induce dissociation of BRCA1 from chromatin, inhibit DNA repair, and promote senescence. Developmental Cell 21(6): 1077-91, 2011.

9. Bitler, B. G., Nicodemus, J. P., Li, H., Cai, Q., Wu, H., Hua, X., Li, T., Birrer, M. J., Godwin, A. K., Cairns, P., Zhang, R.Wnt5a suppresses epithelial ovarian cancer by promoting cellular senescence. Cancer Research 71(19): 6184-94, 2011.

10. Kennedy, A. L., Morton, J. P., Manoharan, I., Nelson, D. M., Jamieson, N. B., Pawlikowski, J. S., McBryan, T., Doyle, B., McKay, C., Oien, K. A., Enders, G. H., Zhang, R., Sansom, O. J., Adams, P. D.Activation of the PIK3CA/AKT pathway suppresses senescence induced by an activated RAS oncogene to promote tumorigenesis. Molecular Cell 42(1): 36-49, 2011.