Journal
EPIGENETICS
Volume 5, Issue 2, Pages 100-104Publisher
LANDES BIOSCIENCE
DOI: 10.4161/epi.5.2.10778
Keywords
prostate cancer; AR; epigenetics; histone demethylase; histone deacetylase
Funding
- Flight Attendant Medical Research Institute and National Institutes of Health through the Oregon Clinical and Translational Research Institute (OCTRI) [1KL2 RR024141 01]
- National Center for Research Resources (NCRR), National Institutes of Health (NIH) [UL1 RR024140]
- NIH Roadmap for Medical Research
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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 nuclear hormone and transcription factor, is the most therapeutically relevant target in this disease. While most efforts in the clinic are still directed at lowering levels of androgens that activate AR, resistance to androgen deprivation eventually develops, and most prostate cancer deaths are attributable to this castration-resistant form of this disease. Recent work has shed light on the importance of epigenetic events including facilitation of AR signaling by histone-modifying enzymes and also on the role that enzymes such as HDAC6 play in stabilizing AR in prostate cancer cells. Herein, we summarize recent findings on the role of epigenetic enzymes in AR signaling and highlight examples on how interdiction of critical epigenetic enzymes may attenuate AR action in prostate cancer.
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