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J. Biol. Chem., Vol. 279, Issue 8, 7119-7130, February 20, 2004

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Epidermal Growth Factor Increases Coactivation of the Androgen Receptor in Recurrent Prostate Cancer^*

Christopher W. Gregory¶, Xiaoyin Fei||, Liliana A. Ponguta¶, Bin He||**, Heather M. Bill¶, Frank S. French||, and Elizabeth M. Wilson||**

From the Laboratories for Reproductive Biology, Lineberger Comprehensive Cancer Center, and the Departments of ^¶Pathology and Laboratory Medicine, ^||Pediatrics, and ^**Biochemistry and Biophysics, University of North Carolina, Chapel Hill, North Carolina 27599-7500

Growth of normal and neoplastic prostate is mediated by the androgen receptor (AR), a ligand-dependent transcription factor activated by high affinity androgen binding. The AR is highly expressed in recurrent prostate cancer cells that proliferate despite reduced circulating androgen. In this report, we show that epidermal growth factor (EGF) increases androgen-dependent AR transactivation in the recurrent prostate cancer cell line CWR-R1 through a mechanism that involves a post-transcriptional increase in the p160 coactivator transcriptional intermediary factor 2/glucocorticoid receptor interacting protein 1 (TIF2/GRIP1). Site-specific mutagenesis and selective MAPK inhibitors linked the EGF-induced increase in AR transactivation to phosphorylation of TIF2/GRIP1. EGF signaling increased the coimmunoprecipitation of TIF2 and AR. AR transactivation and its stimulation by EGF were reduced by small interfering RNA inhibition of TIF2/GRIP1 expression. The data indicate that EGF signaling through MAPK increases TIF2/GRIP1 coactivation of AR transactivation in recurrent prostate cancer.

Received for publication, July 16, 2003 , and in revised form, December 2, 2003.

^* This work was supported by NICHD, National Institutes of Health (NIH), United States Public Health Service Grants HD16910 and HD04466, NCI, NIH, Grant P01 CA77739, United States Army Medical Research and Material Command Grants DAMD17-00-1-0094 and DAMD17-02-1-0110, the International Training and Research in Population and Health Program supported by the Fogarty International Center and NICHD, NIH, and by an unsolicited donation from the Yamanouchi USA Foundation (Washington, D. C.). 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.

To whom correspondence should be addressed: Laboratories for Reproductive Biology, CB# 7500, Rm. 3340C, Medical Biomolecular Research Bldg., 103 Mason Farm Rd., University of North Carolina, Chapel Hill, NC 27599-7500. Tel.: 919-966-5168; Fax: 919-966-2203; E-mail: emw{at}med.unc.edu.

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