Rapid signalling by androgen receptor in prostate cancer cells

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Updated: Oct 18, 2026

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
12:13

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

Published on: November 19, 2019

H Peterziel1, S Mink, A Schonert

  • 1Forschungszentrum Karlsruhe, Institut für Toxikologie und Genetik, Germany.

Oncogene
|December 22, 1999
PubMed

Insights

Androgen receptors regulate prostate cancer growth. Beyond gene expression, they rapidly activate mitogen-activated protein kinases (MAPKs), influencing cellular signaling pathways through non-transcriptional actions.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Androgens are key regulators of prostate cancer growth.
  • The androgen receptor (AR) typically acts by binding androgens, translocating to the nucleus, and modulating gene expression.
  • Prostate cancer cells are androgen-responsive, making AR a critical therapeutic target.

Purpose of the Study:

  • To investigate novel modes of androgen receptor (AR) action in prostate cancer cells.
  • To explore non-transcriptional signaling pathways regulated by the AR.
  • To understand the rapid signaling effects of androgens beyond gene regulation.

Main Methods:

  • Treatment of androgen-responsive prostate cancer cells with dihydrotestosterone.
  • Transient transfection assays to assess transcription factor activity.
  • Biochemical studies and dominant-negative mutant analyses to identify involved kinases.

Main Results:

  • Dihydrotestosterone rapidly and reversibly activated mitogen-activated protein kinases (MAPKs/Erks) in prostate cancer cells.
  • AR-mediated MAPK activation enhanced the activity of the transcription factor Elk-1.
  • This AR action was rapid and insensitive to common androgen antagonists (e.g., hydroxyflutamide, casodex).
  • Kinases including MAPK/Erk kinase, phosphatidyl-inositol 3-kinase, and protein kinase C were involved in AR-mediated MAPK activation.

Conclusions:

  • The androgen receptor (AR) exhibits a novel mode of action in prostate cancer cells, distinct from its canonical transcriptional role.
  • AR rapidly modulates cellular signaling by activating MAPKs through non-transcriptional mechanisms.
  • These findings reveal that AR utilizes non-conventional pathways to influence cellular processes, offering new insights into prostate cancer regulation.

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