Increased androgen receptor transcription: A cause of castration-resistant prostate cancer and a possible therapeutic target

Masaki Shiota, Akira Yokomizo, Seiji Naito

研究成果: ジャーナルへの寄稿総説査読

79 被引用数 (Scopus)

抄録

Few effective therapies exist for the treatment of castration-resistant prostate cancer (CRPC). Recent evidence suggests that CRPC may be caused by augmented androgen/androgen receptor (AR) signaling, generally involving AR overexpression. Aberrant androgen/AR signaling associated with AR overexpression also plays a key role in prostate carcinogenesis. Although AR overexpression could be attributed to gene amplification, only 10-20% of CRPCs exhibit AR gene amplification, and aberrant AR expression in the remaining instances of CRPC is thought to be attributed to transcriptional, translational, and post-translational mechanisms. Overexpression of AR at the protein level, as well as the mRNA level, has been found in CRPC, suggesting a key role for transcriptional regulation of AR expression. Since the analysis of the AR promoter region in the 1990s, several transcription factors have been reported to regulate AR transcription. In this review, we discuss the molecules involved in the control of AR gene expression, with emphasis on its transcriptional control by transcription factors in prostate cancer. We also consider the therapeutic potential of targeting AR expression.

本文言語英語
ページ(範囲)R25-R41
ジャーナルJournal of Molecular Endocrinology
47
1
DOI
出版ステータス出版済み - 8月 2011

!!!All Science Journal Classification (ASJC) codes

  • 分子生物学
  • 内分泌学

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