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RAS pathways in prostate cancer - mediators of hormone resistance?

Hayley C Whitaker1, David E Neal

  • 1Uro-Oncology Research Group, Cancer Research UK Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge, CB2 0RE, UK. Hayley.Whitaker@cancer.org.uk

Current Cancer Drug Targets
|August 20, 2010
PubMed

Insights

Ras isoforms are crucial in prostate cancer progression, influencing androgen receptor activity in both hormone-sensitive and independent stages. Targeting Ras offers a potential therapeutic strategy for prostate cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Ras isoforms, though infrequently mutated, are critical in prostate cancer.
  • They influence androgen receptor (AR) activity and coregulator function via post-translational modifications.
  • Ras signaling is implicated in prostate cancer progression to androgen independence.

Purpose of the Study:

  • To review the evidence for Ras isoforms as a therapeutic target in prostate cancer.
  • To highlight Ras's role in both androgen-dependent and independent prostate cancer.

Main Methods:

  • Literature review of studies investigating Ras pathways in prostate cancer.
  • Analysis of Ras isoform involvement in AR activation and prostate tumorigenesis.

Main Results:

  • Ras is required for AR activation in hormone-sensitive prostate cancer cells.
  • Ras synergizes with other pathways to promote prostate tumorigenesis.
  • Ras plays a pivotal role in pathways driving progression to androgen independence.

Conclusions:

  • Ras isoforms are implicated in multiple critical pathways in prostate cancer.
  • Ras represents a promising therapeutic target for both androgen-dependent and independent prostate cancer.

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