Related Experiment Video

Updated: Jan 26, 2026

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

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Transcriptional repression by androgen receptor: roles in castration-resistant prostate cancer

Galina Gritsina1, Wei-Qiang Gao2, Jindan Yu1,3,4

  • 1Division of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

Asian Journal of Andrology
|April 6, 2019
PubMed

Insights

Androgen receptor (AR) represses gene expression, a role crucial in prostate cancer progression. Understanding AR

Area of Science:

  • Oncology and Molecular Biology

Background:

  • Androgen receptor (AR) is a key factor in prostate cancer progression and a therapeutic target.
  • Androgen-deprivation therapies can lead to castration-resistant prostate cancer (CRPC) and neuroendocrine prostate cancer (NEPC).
  • CRPC relies on AR signaling, while NEPC involves AR-repressed genes.

Purpose of the Study:

  • To review the molecular mechanisms of AR-mediated gene repression.
  • To summarize AR-repressed genes upregulated in CRPC and NEPC.
  • To identify potential therapeutic targets based on AR's repressive function.

Main Methods:

  • Review of recent literature on AR function and genome-wide analyses.
  • Analysis of AR's role as a transcriptional repressor.
  • Compilation of data on AR-repressed genes in prostate cancer subtypes.

Main Results:

  • AR functions not only as an activator but also as a transcriptional repressor.
  • Genome-wide studies reveal numerous AR target genes.
  • Specific AR-repressed genes are aberrantly upregulated in CRPC and NEPC.

Conclusions:

  • AR's repressive function is critical in prostate cancer development and progression.
  • AR-repressed genes represent promising therapeutic targets for CRPC and NEPC.
  • Further research into AR's repressive mechanisms can guide novel treatment strategies.
Keywords:
CRPCEZH2NEPCandrogen receptorhistone modificationstargeted therapytranscriptional repressor

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