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Updated: May 23, 2026

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors
12:03

Receptor Autoradiography Protocol for the Localized Visualization of Angiotensin II Receptors

Published on: June 7, 2016

Therapeutic targeting of angiotensin II receptor type 1 to regulate androgen receptor in prostate cancer

Satoru Takahashi1, Hiroji Uemura, Azman Seeni

  • 1Department of Experimental Pathology and Tumor Biology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan. sattak@med.nagoya-cu.ac.jp

The Prostate
|March 21, 2012
PubMed
Abstract

Insights

Angiotensin II receptor blockers (ARBs) show promise in preventing and treating prostate cancer. These drugs, including telmisartan and candesartan, reduced tumor growth in rats and prolonged prostate-specific antigen (PSA) progression in patients.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Limited curative options for castration-resistant prostate cancer (CRPC) drive research into prostate cancer prevention.
  • Angiotensin II receptor blockers (ARBs) may reduce prostate-specific antigen (PSA) levels and improve CRPC patient outcomes.
  • Investigating the direct impact of ARBs on prostate cancer growth and progression is crucial.

Purpose of the Study:

  • To evaluate the chemopreventive and chemotherapeutic potential of ARBs in prostate cancer.
  • To determine the effects of ARBs on prostate cancer growth, progression, and underlying molecular mechanisms.

Main Methods:

  • Utilized the Transgenic Rat for Adenocarcinoma of Prostate (TRAP) model, administering ARBs (telmisartan, candesartan) orally.
  • Conducted in vitro studies using LNCaP cells to assess cell growth, ubiquitylation, and reporter gene activity.
  • Performed microarray analysis to identify molecular changes induced by ARB treatment.

Main Results:

  • ARBs (telmisartan, candesartan) attenuated prostate carcinogenesis in TRAP rats by increasing apoptosis via caspase activation, p38 MAPK inactivation, and androgen receptor (AR) down-regulation.
  • Microarray analysis revealed ARB-induced up-regulation of estrogen receptor β (ERβ).
  • ARBs inhibited cell growth and AR-mediated transcriptional activity in LNCaP cells, with a modest additive effect via ERβ up-regulation. An intervention study showed prolonged PSA progression in patients receiving ARBs.

Conclusions:

  • ARBs demonstrate significant potential as chemopreventive agents against prostate cancer.
  • ARBs show promise as chemotherapeutic agents for prostate cancer, impacting key signaling pathways.
  • The findings suggest a novel therapeutic strategy utilizing ARBs for prostate cancer management.

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