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Updated: Jun 12, 2026

Murine Prostate Micro-dissection and Surgical Castration
08:49

Murine Prostate Micro-dissection and Surgical Castration

Published on: May 11, 2016

Estradiol suppresses tissue androgens and prostate cancer growth in castration resistant prostate cancer

Bruce Montgomery1, Peter S Nelson, Robert Vessella

  • 1Department of Medicine, University of Washington School of Medicine, 1959 NE Pacific St, Seattle, WA, USA. rbmontgo@u.washington.edu

BMC Cancer
|June 1, 2010
PubMed
Abstract

Insights

Estrogen therapy effectively inhibits castration-resistant prostate cancer (CRPC) growth by reducing tumoral androgens, independent of estrogen receptors. This finding offers new strategies for CRPC treatment.

Area of Science:

  • Oncology
  • Endocrinology
  • Cancer Biology

Background:

  • Prostate cancer can progress to castration-resistant prostate cancer (CRPC) even with low serum androgen levels.
  • The mechanisms by which estrogens suppress CRPC growth in the absence of androgens are not fully understood.
  • Estrogen's potential role in CRPC may be independent of the estrogen receptor.

Purpose of the Study:

  • To investigate the hypothesis that estrogen inhibits CRPC in orchiectomized animals by suppressing tumoral androgens.
  • To determine if this effect is independent of the estrogen receptor.

Main Methods:

  • Human CRPC xenografts (LuCaP 35V) were implanted into male SCID mice.
  • Tumors were treated with placebo, 17beta-estradiol, or 17beta-estradiol plus an estrogen receptor antagonist (ICI 182,780).
  • Tumor growth, survival rates, and tissue levels of testosterone (T) and dihydrotestosterone (DHT) were evaluated using mass spectrometry.

Main Results:

  • 17beta-estradiol significantly slowed tumor growth and improved survival in CRPC xenografts.
  • The estrogen receptor antagonist ICI 182,780 did not alter the effects of 17beta-estradiol on growth or survival.
  • 17beta-estradiol markedly suppressed intratumoral T and DHT levels, irrespective of ICI 182,780 presence.

Conclusions:

  • CRPC maintains intratumoral androgen levels despite castration.
  • Estrogen inhibits CRPC growth through an estrogen receptor-independent suppression of tumor T and DHT.
  • Targeting tissue steroidogenesis is a promising strategy for developing novel CRPC therapies.

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