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Updated: Feb 12, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
07:25

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

Published on: March 6, 2018

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A Novel Mechanism to Drive Castration-Resistant Prostate Cancer

Salma Kaochar1, Nicholas Mitsiades1

  • 1Department of Medicine, Baylor College of Medicine, Houston, TX 77030, USA; Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.

Trends in Endocrinology and Metabolism: TEM
|April 2, 2018
PubMed

Insights

Prostate cancer relies on androgen receptor signaling. Researchers found that a reduced androgen-inactivating enzyme increases local androgens, promoting cancer growth even after treatment.

Area of Science:

  • Oncology
  • Endocrinology
  • Molecular Biology

Background:

  • Androgen receptor (AR) signaling is a key driver in prostate adenocarcinoma development and progression.
  • Despite androgen deprivation therapy (ADT), persistent intratumoral androgens contribute to castration-resistant prostate cancer (CRPC).
  • Increased in situ androgen synthesis is a known mechanism for intratumoral androgen persistence.

Purpose of the Study:

  • To investigate alternative mechanisms contributing to local androgenic exposure in prostate cancer.
  • To identify factors that enhance androgen availability in the tumor microenvironment, particularly in the context of CRPC.

Main Methods:

  • The study focused on the role of androgen-inactivating enzymes.
  • Investigated the impact of enzyme downregulation on local androgen levels.
  • Utilized findings from Sharifi and colleagues' recent report.

Main Results:

  • A novel mechanism enhancing local androgenic exposure was identified.
  • Downregulation of a specific androgen-inactivating enzyme was found to increase androgen levels within the tumor.
  • This enzymatic shift contributes to AR signaling in prostate cancer.

Conclusions:

  • Reduced activity of androgen-inactivating enzymes represents a significant mechanism for increased local androgen availability in prostate cancer.
  • Targeting these enzymes could offer new therapeutic strategies for managing CRPC.
  • Understanding these pathways is crucial for overcoming treatment resistance.
Keywords:
DHTHSD17B4 variant 2androgen receptor (AR) signalingcastration-resistant prostate cancertestosterone

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