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Mechanisms of the androgen receptor splicing in prostate cancer cells

L L Liu1, N Xie1, S Sun2

  • 1Department of Urologic Sciences, Vancouver Prostate Centre, University of British Columbia, Vancouver, British Columbia, Canada.

Oncogene
|July 16, 2013
PubMed

Insights

Androgen deprivation therapy resistance in prostate cancer involves androgen receptor (AR) splice variants. This study reveals ADT increases AR gene transcription and splicing factor recruitment, enhancing AR-V7 production.

Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • Prostate tumors develop resistance to androgen deprivation therapy (ADT) through mechanisms including constitutively active androgen receptor (AR) splice variants.
  • AR splice variant 7 (AR-V7) is a key driver of prostate tumor progression under ADT, but its generation mechanism is unclear.

Purpose of the Study:

  • To elucidate the molecular mechanism behind AR-V7 generation in prostate cancer cells under ADT.
  • To investigate the relationship between AR gene transcription, RNA splicing, and AR-V7 production.

Main Methods:

  • Analysis of AR gene transcription initiation and elongation rates under ADT.
  • Assessment of RNA splicing factor recruitment to AR pre-mRNA.
  • Identification of RNA splicing enhancers and binding proteins involved in AR-V7 formation.

Main Results:

  • ADT enhances AR gene transcription, creating conditions for increased AR pre-mRNA and splicing factor interactions.
  • Recruitment of specific RNA splicing factors to the 3' splicing site for AR-V7 is increased under ADT.
  • Two RNA splicing enhancers and their binding proteins (U2AF65 and ASF/SF2) were identified as critical for AR-V7 splicing.

Conclusions:

  • ADT-induced increases in AR gene transcription rate contribute to enhanced AR-V7 levels.
  • Increased splicing factor recruitment to AR pre-mRNA is a key mechanism for AR-V7 generation.
  • Understanding these mechanisms offers potential therapeutic targets for overcoming ADT resistance in prostate cancer.

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