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J. Biol. Chem., Vol. 278, Issue 33, 30605-30613, August 15, 2003

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Differential Requirement of SWI/SNF for Androgen Receptor Activity^*

Thomas W. Marshall, Kevin A. Link, Christin E. Petre-Draviam  and Karen E. Knudsen 

From the Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0521

The androgen receptor (AR) is a ligand-dependent transcription factor whose activity is required for prostate cancer proliferation. Because ablation of AR activity is a critical goal of prostate cancer therapy, much emphasis has been placed on understanding the accessory proteins that regulate AR function in the prostate. Several co-activators have been shown to be required for full AR activity, including histone acetyl-transferases and TRAP/mediator complexes. SWI/SNF comprises a family of large, multisubunit complexes present in the cell, which contain one of two core ATPases required for nucleosome re-positioning, BRG1 or hBRM. We investigated the specific requirement of the SWI/SNF core ATPases for AR function. Using cells deficient in both BRG1 and hBRM, we show that activation of one AR target promoter, prostate-specific antigen (PSA), requires SWI/SNF chromatin remodeling for activity. A second AR target promoter, probasin, maintained a low level of activation in the absence of SWI/SNF. AR stimulation on the probasin core promoter could be partially induced with BRG1, but hBRM strongly stimulated AR activity. The PSA promoter was only induced by the restoration of hBRM. In contrast, ligand-dependent activation of the estrogen receptor was equally stimulated by BRG1 or hBRM. We demonstrate that the addition of a known enhancer region to the core PSA promoter bypasses the requirement for SWI/SNF on the PSA promoter, indicating that elements upstream of specific proximal promoters can impact the influence of the SWI/SNF complex on target gene activation. Addition of the enhancer to the probasin core promoter failed to impact the SWI/SNF requirement. In summary, SWI/SNF function potently regulates core AR target gene promoter activation, with a preference for hBRM-containing complexes. These studies highlight a role for the enhancer in altering the impact of SWI/SNF action and suggest a disparity in AR target genes for SWI/SNF requirement.

Received for publication, May 1, 2003 , and in revised form, May 28, 2003.

^* This work was supported in part by Department of Defense Grant DAMD-02-1-0037 (to K. E. K.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Supported by the Albert J. Ryan Foundation and the University of Cincinnati Distinguished Graduate Award.

To whom correspondence should be addressed. Tel.: 513-558-7371; Fax: 513-558-4454; E-mail: Karen.Knudsen{at}UC.edu.

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