Related Experiment Video

Updated: Nov 22, 2025

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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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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Loss and revival of androgen receptor signaling in advanced prostate cancer

Nicolò Formaggio1, Mark A Rubin2, Jean-Philippe Theurillat3

  • 1Institute of Oncology Research, Università della Svizzera italiana, Lugano, Switzerland.

Oncogene
|January 9, 2021
PubMed

Insights

Stronger prostate cancer treatments targeting the androgen receptor (AR) can cause AR-negative disease, which has a poor prognosis. This review explores mechanisms of this transition and strategies to maintain AR-dependence.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Androgen receptor (AR) signaling is a primary target in prostate cancer therapy.
  • Advanced anti-androgen therapies have improved treatment outcomes.
  • However, intensified AR pathway inhibition can drive prostate cancer dedifferentiation to an AR-negative state.

Purpose of the Study:

  • To review the molecular mechanisms underlying the transition from AR-positive to AR-negative prostate cancer.
  • To discuss current strategies aimed at preventing or reversing this dedifferentiation process.
  • To explore methods for maintaining or restoring AR-dependence in prostate cancer.

Main Methods:

  • Literature review of molecular mechanisms in prostate cancer progression.
  • Analysis of studies on AR signaling pathway inhibition.
  • Synthesis of research on therapeutic strategies for AR-negative prostate cancer.

Main Results:

  • Dedifferentiation to AR-negative disease is a consequence of potent AR signaling blockade.
  • This transition is associated with aggressive tumor behavior and poor patient prognosis.
  • Specific molecular pathways facilitate the switch from AR-positive to AR-negative phenotypes.

Conclusions:

  • Understanding the mechanisms of AR-negative prostate cancer development is crucial.
  • Developing strategies to prevent or revert AR-dependence is a key therapeutic challenge.
  • Maintaining AR-dependence may offer a path to improved long-term outcomes for prostate cancer patients.

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