期刊
ENDOCRINE-RELATED CANCER
卷 21, 期 5, 页码 R395-R407出版社
BIOSCIENTIFICA LTD
DOI: 10.1530/ERC-14-0217
关键词
androgen receptor; cell signaling; chemotherapy; endocrine therapy resistance; oncogene
资金
- National Cancer Institute [R01 CA124706, R01 CA178338]
- Paul Mellon Urologic Cancer Institute
It is increasingly clear that castration-resistant prostate cancer (PCa) is dependent on the androgen receptor (AR). This has led to the use of anti-androgen therapies that reduce endogenous steroid hormone production as well as the use of AR antagonists. However, the AR does not act in isolation and integrates with a milieu of cell-signaling proteins to affect cell biology. It is well established that cancer is a genetic disease resulting from the accumulation of mutations and chromosomal translocations that enables cancer cells to survive, proliferate, and disseminate. To maintain genomic integrity, there exists conserved checkpoint signaling pathways to facilitate cell cycle delay, DNA repair, and/or apoptosis in response to DNA damage. The AR interacts with, affects, and is affected by these DNA damage-response proteins. This review will focus on the connections between checkpoint signaling and the AR in PCa. We will describe what is known about how components of checkpoint signaling regulate AR activity and what questions still face the field.
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