Related Experiment Video

Updated: Sep 7, 2025

Detecting the Ligand-binding Domain Dimerization Activity of Estrogen Receptor Alpha Using the Mammalian Two-Hybrid Assay
09:07

Detecting the Ligand-binding Domain Dimerization Activity of Estrogen Receptor Alpha Using the Mammalian Two-Hybrid Assay

Published on: December 19, 2018

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The Androgen Hormone-Induced Increase in Androgen Receptor Protein Expression Is Caused by the Autoinduction of the

Tiziana Siciliano1, Ulrich Sommer2, Alicia-Marie K Beier1,3

  • 1Department of Urology, Technische Universität Dresden, 01307 Dresden, Germany.

Current Issues in Molecular Biology
|June 20, 2022
PubMed

Insights

High androgen levels inhibit prostate cancer cell growth by increasing androgen receptor (AR) activity and stability. Therapeutic reduction of androgens may decrease AR activity, slowing prostate cancer progression.

Area of Science:

  • Androgen receptor (AR) signaling in prostate cancer
  • Molecular mechanisms of prostate cancer progression

Background:

  • The androgen receptor (AR) is crucial in prostate, muscle, bone, and adipose tissues.
  • Dysregulated AR activity drives prostate cancer (PCa) initiation and progression.
  • Antiandrogenic therapy is a key PCa treatment, but high androgens also inhibit PCa cells.

Purpose of the Study:

  • Investigate the effects of varying androgen concentrations on PCa cell viability.
  • Analyze AR localization, transactivation, and protein stability under different androgen levels.
  • Elucidate the molecular mechanisms behind high androgen-induced inhibition of PCa cell growth.

Main Methods:

  • Cell viability assessed using WST1 assay.
  • AR transactivity evaluated by qPCR analysis of AR target genes.
  • AR localization visualized using fluorescent AR fusion protein microscopy.
  • AR protein expression changes detected by Western blot.

Main Results:

  • High androgen concentrations reduced viability in LNCaP and C4-2 PCa cell lines.
  • Androgens increased AR transactivity, localization, and protein expression.
  • High androgen levels did not decrease these AR parameters but induced increased AR protein synthesis.
  • Inhibitory effects on cell viability are linked to AR downstream signaling or non-genomic AR activity.

Conclusions:

  • Hormonal activation of the AR leads to self-induced receptor stabilization and increased activity.
  • High androgen levels inhibit PCa cell viability through AR downstream signaling or non-genomic activity.
  • Therapeutic reduction of androgen levels is a potential clinical strategy to decrease AR activity and slow PCa progression.
Keywords:
biphasic effect of androgensprotein stabilitytestosterone

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