Rugang Zhang, Ph.D.
Rugang Zhang, Ph.D.
- Associate Professor, 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.
1. Bitler BG, Garipov A, Amatangelo M, Kossenkov A, Schultz DC, Shih IM, Conejo-Garcia JR, Speicher DW, Zhang R. Targeting EZH2 methyltransferase activity in ARID1A mutated cells is synthetic lethal. Nature Medicine; 2015: In Press.
2. 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; 2015: In Press.
3. 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.
4. Tu Z, Zhuang X, Yao YG, Zhang R. BRG1 is required for formation of senescence-associated heterochromatin foci induced by oncogenic RAS or BRCA1 loss. Molecular and Cellular Biology; 33: 1819-1829, 2013.
5. Garipov A, Li H, Thapa RJ, Balachandran S, Zhang R. NF-YA underlies EZH2 upregulation and is essential for proliferation of human epithelial ovarian cancer cells. Molecular Cancer Research; 11: 360-369, 2013.
6. Li H, Bitler BG, Maradeo ME, Slifker M, Vathipadiekal V, Careasy C, Tummino P, Cairns P, Birrer MJ, Zhang R. ALDH1A1 is a novel EZH2 target gene in epithelial ovarian cancer identified by genome-wide approaches. Cancer Prevention Research; 5: 484-91, 2012.
7. Tu Z, Nicodemus J, Beehary N, Xia B, Yen T, and Zhang R. Oncogenic Ras regulates BRIP1 expression to induce dissociation of BRCA1 from chromatin, inhibit DNA repair, and promote senescence. Developmental Cell; 21: 1077-91, 2011.
8. Kennedy AL, Morton JP, Manoharan I, Nelson DM. Jamieson NB, Pawlikowski JS, McBryan T, Doyle B, Oien KA, Enders GH, Zhang R, Sansom OJ, Adams PD. Activation of the PI3K3CA/AKT pathway suppresses senescence induced by an activated RAS oncogene to promote tumorigenesis. Molecular Cell; 42: 36-49, 2011.
9. Bitler BG, Nicodemus JP, Li H, Cai Q, Wu H, Hua X, Li T, Birrer MJ, Godwin AK, Cairns P, Zhang R. Wnt5a suppresses epithelial ovarian cancer by promoting cellular senescence. Cancer Research; 71:6184-94, 2011.
10. Li H, Cai Q, Godwin AK, Zhang R. Enhancer of zeste homology 2 promotes the proliferation and invasion of human epithelial cells. Molecular Cancer Research; 8: 1610-1618, 2010.