Qianben Wang

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Assistant Professor

Ph.D. - University of Maryland School of Medicine
Post Doctoral - Dana-Farber Cancer Institute and Harvard Medical School

Androgens, functioning through androgen receptor (AR), are essential for the initiation and progression of prostate cancer. Thus androgen-ablation therapies, which involve surgical castration or the use of luteinizing hormone-releasing hormone (LHRH) agonists (or antagonists), have been the mainstay of treatment for advanced androgen-dependent prostate cancer (ADPCa) for over 40 years. While such therapies initially lead to disease regression, in general, advanced prostate cancer ultimately progresses to an androgen-independent prostate cancer (AIPCa) late stage that is refractory to current therapies. My laboratory is interested in understanding the molecular pathological mechanisms underlying the development and progression of prostate cancer. As AR is expressed in the vast majority of both ADPCa and AIPCa, and decreasing levels of AR protein expression reduces both ADPCa and AIPCa growth in model systems, it appears AR signaling pathways play a critical role in both ADPCa and AIPCa.

AR is a ligand-dependent transcription factor belonging to the nuclear hormone receptor (NR) superfamily. The application of chromatin immunoprecipitation (ChIP) to study protein-DNA interaction has provided a wealth of information on temporal and spatial assembly of AR transcription complex on target gene regulatory regions in vivo. However, studying of only a few target genes by ChIP greatly limits our understanding of how AR regulates target gene network. The recent development of the ChIP-on-chip (ChIP on a microarray) or ChIP-seq (ChIP combined with high throughput sequencing) technique allows the global identification of specific transcription factor regulatory regions across the human genome. Recently, we have mapped AR binding regions in the entire human genome in ADPCa and AIPCa. By combining the AR binding maps with gene expression profiles, we have begun to understand how AR regulates target gene networks in ADPCa and AIPCa. Currently, we are extending our view from transcriptional regulation by AR to wider transcriptional regulations in prostate cancer including studying combinatorial transcriptional regulation by AR, its collaborating transcription factors, and its coactivators. We will also apply the genome-wide ChIP technique to clinical samples obtained from different stages of prostate cancer. This would allow identification of critical cis-regulatory sequences contributing to prostate cancer progression.

Recent Publications:

• Wang Q, Li W, Zhang Y, Yuan X, Xu K, Yu J, Chen Z, Beroukhim R, Wang H, Wu T, et al (2009) "Androgen receptor regulates a distinct transcription program in androgen-independent prostate cancer" Cell 138:245-56. (Featured Article).
• Frigo DE, Sherk AB, Wittmann BM, Norris JD, Wang Q, Joseph JD, Toner AP, Brown M, McDonnell DP (2009) "Induction of Kruppel-like factor 5 expression by androgens results in increased CXCR4-dependent migration of prostate cancer cells in vitro" Mol Endocrinol. 23(9):1385-96.
• Sun T, Wang Q, Balk SP, Brown M, Lee GS and Kantoff PW (2009) "Roles of microRNA-221 and -222 in castration resistant prostate cancer" Cancer Res 69:3356-63.
• Wang Q and Brown M (2009) "Mapping the androgen receptor cistrome" In Tindall DJ and Mohler JL, eds. Androgen Action in Prostate Cancer, New York, NY: Springer Science and Business Media, pp.663-80.
• Nwachukwu JC, Mita P, Ruoff R, Ha S, Wang Q, Huang SJ, Taneja SS, Brown M, Gerald WL, Garabedian MJ and Logan SK (2009) "Genome-wide impact of androgen receptor trapped clone-27 loss on androgen-regulated transcription in prostate cancer cells" Cancer Res 69(7):3140-7.
• Frigo DE, Sherk AB, Wittmann BM, Norris JD, Wang Q, Joseph JD, Toner AP, Brown M, McDonnell DP (2009) "Induction of Kruppel-like factor 5 expression by androgens results in increased CXCR4-dependent migration of prostate cancer cells in vitro" Mol Endocrinol 2009 May 21. [Epub ahead of print]
• Lupien M, Eeckhoute J, Meyer CA, Wang Q, Zhang Y, Carroll JS, Liu XS, and Brown M (2008) "FoxA1 translates epigenetic signatures into lineage-specific transcription" Cell 132:958-70.
• Bao BY, Chuang BF, Wang Q, Kantoff PW, Brown M, Sartor O, and Lee GS (2008) "Regulation of UGT2B15/17 by androgen signaling in prostate cancer cells" Prostate 68:839-48.
• Agoulnik IU, Bingman WE 3rd, Nakka M, Li W, Wang Q, Liu XS, Brown M, Weigel NL (2008) "Target gene-specific regulation of androgen receptor activity by p42/p44 mitogen-activated protein kinase" Mol Endocrinol 22: 2420-32.
• Wang Q, Li W, Liu XS, Carroll JS, Jänne OA, Keeton EK, Chinnaiyan AM, Pienta KJ and Brown M (2007) "A hierarchical network of transcription factors governs androgen receptor dependent prostate cancer growth" Mol Cell 27:380-92 (Featured Article).
• Wang QF, Prabhakar S, Wang Q, Moses AM, Chanan S, Brown M, Eisen MB, Cheng JF, Rubin EM, and Boffelli D (2006) "Primate-specific evolution of an LDLR enhancer" Genome Biol 7: R68.
• Carroll JS, Meyer CA, Song J, Li W, Brodsky AS, Geistlinger TR, Eeckhoute J, Keeton EK, Fertuck KC, Hall GF, Wang Q, Bekiranov S, Sementchenko V, Fox EA, Silver PA, Gingeras TR, Liu XS and Brown M (2006) "Genome wide analysis of estrogen receptor binding sites" Nat Genet 38:1289-97.
• Wang Q, Carroll JS and Brown M (2005) "Spatial and temporal recruitment of androgen receptor and its coactivators involves chromosomal looping and polymerase tracking" Mol Cell 19:631-42.
• Wang Q, Udayakumar TS, Vasaitis TS, Brodie AH and Fondell JD(2004) "Mechanistic relationship between androgen receptor polyglutamine tract truction and androgen-dependent transcriptional hyperactivity in prostate cancer cells" J Biol Chem 279:17319-28.
• Wang Q, Dipali S, Ren Y and Fondell JD (2002) "A coregulatory role for the TRAP-Mediator complex in androgen receptor-mediated gene expression" J Biol Chem 277:42852-58