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07:25

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Disruption of androgen receptor function inhibits proliferation of androgen-refractory prostate cancer cells

Ofelia L Zegarra-Moro1, Lucy J Schmidt, Haojie Huang

  • 1Department of Biochemistry, Mayo Clinic, Rochester, Minnesota 55905, USA.

Cancer Research
|February 28, 2002
PubMed

Insights

Prostate cancer cells require androgen receptors (AR) for growth. Even when androgens are absent, blocking AR stops the proliferation of refractory prostate cancer cells, showing AR

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • Prostate cancer growth is driven by androgens and the androgen receptor (AR).
  • Tumors often become androgen-refractory after treatment, indicating a need to understand resistance mechanisms.

Purpose of the Study:

  • To investigate the role of the androgen receptor (AR) in the proliferation of androgen-refractory prostate cancer cells.

Main Methods:

  • Used an antibody and an AR mRNA hammerhead ribozyme to disrupt AR activity.
  • Tested effects on androgen-sensitive (LNCaP), androgen-refractory (LNCaP-Rf, LNCaP-C4), and androgen-insensitive (DU-145) prostate cancer cell lines.

Main Results:

  • Disrupting AR activity with either the antibody or ribozyme inhibited proliferation in androgen-refractory cells.
  • AR remains critical for the growth of these refractory cells, even without androgens.

Conclusions:

  • The androgen receptor (AR) is essential for the proliferation of androgen-refractory prostate cancer cells.
  • Targeting AR may be a viable strategy for treating refractory prostate cancer, irrespective of androgen levels.

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