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Updated: Jun 2, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
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Regulation of androgen receptor expression through angiotensin II type 1 receptor in prostate cancer cells

Koji Hoshino1, Hitoshi Ishiguro, Jun-Ichi Teranishi

  • 1Department of Urology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

The Prostate
|May 5, 2011
PubMed
Abstract

Insights

Inhibition of the angiotensin II type 1 receptor (AT1R) significantly reduces prostate cancer cell growth by decreasing androgen receptor (AR) expression. This suggests AT1R as a potential therapeutic target for prostate cancer treatment.

Area of Science:

  • Molecular Biology
  • Oncology
  • Endocrinology

Background:

  • The prostate gland's local renin-angiotensin system (RAS) influences cell proliferation and angiogenesis, but mechanisms are unclear.
  • The role of the angiotensin II type 1 receptor (AT1R) in prostate cancer, particularly its effect on androgen receptor (AR) expression, requires further investigation.

Purpose of the Study:

  • To investigate the impact of AT1R on androgen receptor (AR) expression in prostate cancer cells.
  • To elucidate the molecular mechanisms linking AT1R signaling to AR modulation and prostate cancer cell proliferation.

Main Methods:

  • Western blot, luciferase assays, and immunocytochemistry were used to assess AR modulation by AT1R.
  • siRNA-mediated inhibition of AT1R and angiotensin II (Ang-II) treatment were employed in cell culture models.
  • Quantitative real-time PCR was performed on angiotensinogen or AT1R knockout (KO) mice to evaluate AR expression.

Main Results:

  • Angiotensin II (Ang-II) stimulation enhanced AR, prostate specific antigen (PSA), NF-κB, and c-myc expression, promoting cell proliferation.
  • AT1R inhibition via siRNA decreased LNCaP cell proliferation by 75% and suppressed AR, PSA, NF-κB, and c-myc.
  • AT1R inhibition reduced nuclear translocation of AR, and AT1R KO mice exhibited decreased prostate AR expression.

Conclusions:

  • AT1R inhibition significantly reduces prostate cancer cell growth and AR protein levels.
  • AT1R modulates AR transcriptional activity through effects on NF-κB and c-myc.
  • Targeting AT1R offers a promising strategy for developing novel prostate cancer therapeutics.

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