Document Type

Article

Publication Date

10-12-2011

Comments

This article has been peer reviewed. It was published in: Prostate cancer.

2011; 2011: 918707. .

The published version is available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3196248/. DOI: 10.1155/2011/918707.

Copyright © 2011 A. M. Godbole and V. C. O. Njar.

Abstract

Prostate cancer is the most common cancer in men in the United States, and it is the second leading cause of cancer-related death in American men. The androgen receptor (AR), a receptor of nuclear family and a transcription factor, is the most important target in this disease. While most efforts in the clinic are currently directed at lowering levels of androgens that activate AR, resistance to androgen deprivation eventually develops. Most prostate cancer deaths are attributable to this castration-resistant form of prostate cancer (CRPC). Recent work has shed light on the importance of epigenetic events including facilitation of AR signaling by histone-modifying enzymes, posttranslational modifications of AR such as sumoylation. Herein, we provide an overview of the structure of human AR and its key structural domains that can be used as targets to develop novel antiandrogens. We also summarize recent findings about the antiandrogens and the epigenetic factors that modulate the action of AR.

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