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<center><font face="lucida fax" style= "color:Crimson" size="+10">'''Qianben Wang Laboratory'''</font>
<center><font face="lucida fax" style= "color:yellow" size="+10">'''Qianben Wang Laboratory'''</font>
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<center><font face="lucida fax" style= "color:Crimson" size="+2">'''Laboratory of Cancer Epigenomics'''</font></center>
<center><font face="lucida fax" style= "color:yellow" size="+2">'''Laboratory of Cancer Epigenomics'''</font></center>
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<center><font face="lucida fax" style= "color:Crimson" size="+1">'''Department of Molecular and Cellular Biochemistry, The Ohio State University'''</font>
<center><font face="lucida fax" style= "color:yellow" size="+1">'''Department of Molecular and Cellular Biochemistry, The Ohio State University'''</font>
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[[Wang | <font face="lucida fax" style="color:#ffffff" size="+1"> '''Home''' </font>]] &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;
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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 (ADPC) for over 40 years. While such therapies initially lead to disease regression, in general, advanced prostate cancer ultimately progresses to an castration resistant prostate cancer (CRPC) 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 ADPC and CRPC, and decreasing levels of AR protein expression reduces both ADPC and CRPC growth in model systems, it appears AR signaling pathways play a critical role in both ADPC and CRPC.
My laboratory is interested in understanding the molecular pathological mechanisms underlying the development and progression of prostate cancer. The androgen receptor (AR), a ligand-dependent transcription factor belonging to the nuclear hormone receptor (NR) superfamily, plays a critical role in the onset and progression of prostate cancer. Recently, we have mapped AR binding regions in the entire human genome in prostate cancer cells by using genome-wide chromatin immunoprecipitation (ChIP) techniques. Through an integrated analysis of AR binding and gene expression data, we have begun to understand how AR regulates target genes involved in prostate cancer growth. 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 global ChIP techniques to clinical samples obtained from different stages of prostate cancer. This would allow identification of critical cis-regulatory sequences contributing to prostate cancer progression.
 
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 ADPC and CRPC. By combining the AR binding maps with gene expression profiles, we have begun to understand how AR regulates target gene networks in ADPC and CRPC. 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.
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Revision as of 13:00, 10 November 2011

Qianben Wang Laboratory


Laboratory of Cancer Epigenomics


Department of Molecular and Cellular Biochemistry, The Ohio State University


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My laboratory is interested in understanding the molecular pathological mechanisms underlying the development and progression of prostate cancer. The androgen receptor (AR), a ligand-dependent transcription factor belonging to the nuclear hormone receptor (NR) superfamily, plays a critical role in the onset and progression of prostate cancer. Recently, we have mapped AR binding regions in the entire human genome in prostate cancer cells by using genome-wide chromatin immunoprecipitation (ChIP) techniques. Through an integrated analysis of AR binding and gene expression data, we have begun to understand how AR regulates target genes involved in prostate cancer growth. 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 global ChIP techniques to clinical samples obtained from different stages of prostate cancer. This would allow identification of critical cis-regulatory sequences contributing to prostate cancer progression.

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