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¹ Departments of Cell Biology,
² Center for Environmental Genetics, and
³ UC Cancer Center, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0521, USA

(Requests for offprints should be addressed to K E Knudsen; Email: karen.knudsen{at}uc.edu)

The androgen receptor (AR) mediates the effects of male steroid hormones (androgens) and contributes to a wide variety of physiological and pathophysiological conditions. As such, the regulatory mechanisms governing AR activity are of high significance. Concerted effort has been placed on delineating the mechanisms that control AR activity in prostate cancer, as AR is required for survival and proliferation in this tumor type. Moreover, AR is the central therapeutic target for metastatic prostate cancers, and recurrent tumors evade therapy by restoring AR activity. It is increasingly apparent that AR cofactors which modulate receptor activity can contribute to prostate cancer growth or progression, and this has been particularly well established for AR coactivators. The present review is focused on the role of AR corepressors in governing androgen action, with a specific emphasis on their activities in prostate cancer.

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