Dr. Zhou Wang received his B.S. in biology from the University of Science and Technology of China and his Ph.D. from the University of Pittsburgh. After post-doctoral training at the Carnegie Institution of Washington, Dr. Wang joined the Department of Urology at Northwestern University as an Assistant Professor in 1995 and was honored with the O’Connor Family Research Professorship in 2003. He was relocated to University of Pittsburgh in 2006. Dr. Wang has served as the Director of Urological Research since 2006, a Co-Leader of the Prostate Cancer Program at University of Pittsburgh Cancer Institute (UPCI) from 2006 to 2013, a Co-Leader of the Molecular and Cellular Cancer Biology Program at UPCI from 2014 to 2018, and Director of University of Pittsburgh O’Brien Urology Research Center from 2016-2022. He was a recipient of Junior Faculty Research Award from the American Cancer Society, Edwin Beer Award from the New York Academy of Medicine, SBUR/Merck Young Investigator Award, Jie-Ping Wu Award from Chinese Urology Society, and a MERIT Award from the NIH/NIDDK. Dr. Wang currently holds the UPMC Chair in Urological Research.
Dr. Wang’s research focuses on the mechanisms of androgen action in the prostate and two androgen-dependent diseases, prostate cancer and benign prostatic hyperplasia (BPH), which may lead to improvement of treatment efficacy for patients with prostate cancer and/or BPH. His lab has recently discovered that imported nuclear androgen receptor (AR) does not undergo export and it undergoes nuclear degradation upon androgen withdrawal. This finding is in disagreement with the decades-old paradigm that nuclear AR is exported following androgen withdrawal. His lab has also identified and patented two novel AR antagonists that can inhibit AR nuclear localization; they are nuclear AR degraders (NARDs). His lab was the first to use genetic lineage tracing in the mouse model to show that, in the adult prostate, regenerated luminal epithelial cells are derived from preexisting luminal epithelial cells. His lab has also identified and characterized EAF2/U19, a tumor suppressor regulated by androgens and frequently down-regulated in prostate cancer. In our preclinical/translational studies, the survival of animals bearing androgen-sensitive prostate tumors on intermittent androgen deprivation therapy (IADT) can be significantly prolonged by using short off-cycles coupled with 5a-reductase inhibition. In an effort to explore the molecular mechanisms leading to benign prostatic hyperplasia (BPH), his lab discovered an increased permeability in BPH luminal epithelial cellular junctions. His lab also discovered a 4-fold increase in androgen-responsive gene expression in BPH epithelial cells as compared to the normal adjacent epithelial cells in clinical specimens.