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[Cancer Research 65, 7976-7983, September 1, 2005]
© 2005 American Association for Cancer Research

Endocrinology

SRC-3 Is Required for Prostate Cancer Cell Proliferation and Survival

Hai-Jun Zhou1, Jun Yan1, Weiping Luo5, Gustavo Ayala2,4, Sue-Hwa Lin5, Halime Erdem2, Michael Ittmann2,4, Sophia Y. Tsai1,3 and Ming-Jer Tsai1,3,4

Departments of 1 Molecular and Cellular Biology and 2 Pathology, 3 Program of Development, and 4 Baylor Prostate Cancer Specialized Programs of Research Excellence, Baylor College of Medicine; and 5 Department of Molecular Pathology, University of Texas, M.D. Anderson Cancer Center, Houston, Texas

Requests for reprints: Ming-Jer Tsai, Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030. Phone: 713-798-6253; Fax: 713-798-8227; E-mail: mtsai{at}bcm.tmc.edu.

Prostate cancer is the most common cancer in men in America. Currently, steroid receptor coactivators have been proposed to mediate the development and progression of prostate cancer, at times in a steroid-independent manner. Steroid receptor coactivator-3 (SRC-3, p/CIP, AIB1, ACTR, RAC3, and TRAM-1) is a member of the p160 family of coactivators for nuclear hormone receptors including the androgen receptor. SRC-3 is frequently amplified or overexpressed in a number of cancers. However, the role of SRC-3 in cancer cell proliferation and survival is still poorly understood. In this study, we show that SRC-3 is overexpressed in prostate cancer patients and its overexpression correlates with prostate cancer proliferation and is inversely correlated with apoptosis. Consistent with patient data, we have observed that reduction of SRC-3 expression by small interfering RNA decreases proliferation, delays the G1-S transition, and increases cell apoptosis of different prostate cancer cell lines. Furthermore, with decreased SRC-3 expression, proliferating cell nuclear antigen and Bcl-2 expression, as well as bromodeoxyuridine incorporation in prostate cancer cells are reduced. Finally, knockdown of SRC-3 with inducible short hairpin RNA expression in prostate cancer cells decreased tumor growth in nude mice. Taken together, these findings indicate that SRC-3 is an important regulator of prostate cancer proliferation and survival.




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