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J. Biol. Chem., Vol. 282, Issue 52, 37341-37349, December 28, 2007

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Induction of the SUMO-specific Protease 1 Transcription by the Androgen Receptor in Prostate Cancer Cells^*

Tasneem Bawa-Khalfe¹, Jinke Cheng, Zhengxin Wang^¶, and Edward T. H. Yeh²

From the Research Center for Cardiovascular Diseases, Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, The University of Texas Health Science Center, Houston, Texas 77030 and the Departments of Cardiology and ^¶Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030

Prostate cancer, the most frequently diagnosed carcinoma in males, is readily modulated via the transcriptional activity of androgen receptors. Our recent publication reported that androgen receptor-dependent transcription is significantly elevated with expression of the human sentrin/SUMO-specific protease (SENP1) in the androgen-sensitive human prostate cancer cell line (LNCaP). In situ hybridization studies indicated an elevation of SENP1 message in prostatic intraepithelial neoplasia and prostate cancer lesions as compared with normal prostate epithelia. This study aimed to delineate the mechanism for the regulation of SENP1 message and to determine the pathophysiological consequence of SENP1 induction with respect to prostate cancer. Real-time PCR confirmed the elevation of SENP1 mRNA in prostate cancer cells as compared with normal prostate epithelial cells. Chronic androgen exposure of LNCaP cells prompted an enhancement in the SENP1 transcript selectively. This androgen-mediated augmentation of SENP1 was absent with co-administration of the androgen receptor antagonist bicalutamide and in androgen receptor-negative prostate cancer PC-3 cells, indicating an androgen receptor-dependent event. Activation of the androgen receptor was required for binding an identified androgen response element and positively regulating SENP1 promoter activity. Abrogation of elevated SENP1 mRNA in prostate cancer cells significantly decreased androgen-mediated cell growth. Because increased SENP1 expression directly modulated androgen receptor-dependent cell proliferation and transcription, SENP1 could play an important role in prostate carcinogenesis.

Received for publication, August 21, 2007 , and in revised form, October 3, 2007.

^* This work was supported in part by Department of Defense Grant PC040121 and a prostate cancer development award from the University of Texas MD Anderson Cancer Center (to E. T. H. Y.). 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.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Tables S1 and S2.

¹ Supported in part by National Research Service Award F32-CA110620 from the National Institutes of Health.

² To whom correspondence should be addressed: Dept. of Cardiology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd., Unit 449, Houston, TX 77030. Tel.: 713-792-6242; Fax: 713-745-1942; E-mail: etyeh{at}mdanderson.org.

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