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

Masaki Shiota, Akira Yokomizo, Seiji Naito

Research output: Contribution to journalReview article

63 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)R25-R41
JournalJournal of Molecular Endocrinology
Volume47
Issue number1
DOIs
Publication statusPublished - Aug 1 2011

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Castration
Androgen Receptors
Prostatic Neoplasms
Therapeutics
Gene Amplification
Androgens
Transcription Factors
Genetic Promoter Regions
Prostate
Carcinogenesis

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Endocrinology

Cite this

Increased androgen receptor transcription : A cause of castration-resistant prostate cancer and a possible therapeutic target. / Shiota, Masaki; Yokomizo, Akira; Naito, Seiji.

In: Journal of Molecular Endocrinology, Vol. 47, No. 1, 01.08.2011, p. R25-R41.

Research output: Contribution to journalReview article

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