期刊
INTERNATIONAL JOURNAL OF BIOLOGICAL SCIENCES
卷 7, 期 6, 页码 815-822出版社
IVYSPRING INT PUBL
DOI: 10.7150/ijbs.7.815
关键词
androgen receptor; prostate cancer; splicing variants; alternative splicing
资金
- NIH [CA106504]
- DOD [W81XWH-08-1-0174]
- NATIONAL CANCER INSTITUTE [R01CA106504] Funding Source: NIH RePORTER
Prostate cancer is the second leading cause of cancer-related death in American men. Although most prostate cancers are initially androgen-dependent and respond to androgen ablation therapy, majority of them eventually relapse and progress into incurable castration-resistant (or hormone refractory) prostate cancer. The underlying mechanisms are the focus of intensive investigation for development of more effective treatment. Mounting evidence from both clinical and basic research has demonstrated that the activity of the androgen receptor (AR) is still required for castration-resistant prostate cancer. Multiple mechanisms by which AR is re-activated under androgen-depleted conditions may be involved in the development of castration resistance. The recent identification of AR splicing variants may add another layer of complexity in AR biology. The present review summarizes recent progress in study of AR splicing variants in prostate cancer.
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