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Updated: Dec 28, 2025

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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Androgen receptor-binding sites are highly mutated in prostate cancer

Tunç Morova1,2, Daniel R McNeill3, Nada Lallous2

  • 1School of Medicine, Koç University, Istanbul, 34450, Turkey.

Nature Communications
|February 13, 2020
PubMed

Insights

Prostate cancer frequently mutates androgen receptor (AR) binding sites in non-coding DNA, unlike other transcription factors. These mutations, possibly from faulty DNA repair, can affect tumor growth and enhancer activity.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Androgen receptor (AR) signaling is crucial for most prostate cancers.
  • While AR protein mutations are studied, non-coding AR DNA binding site mutations are less understood.

Purpose of the Study:

  • To investigate somatic mutations at AR binding sites in prostate cancer.
  • To determine if these mutations are specific to prostate cancer and AR, and to identify potential causes.

Main Methods:

  • Analysis of clinical whole genome sequencing data.
  • Comparison of mutation rates at AR binding sites with other transcription factor binding sites.
  • Investigation of estrogen receptor binding sites in breast cancer for comparison.

Main Results:

  • AR binding sites show a significantly elevated mutation rate, exceeding other transcription factors and specific to prostate cancer.
  • Estrogen receptor binding sites also exhibit increased mutations in breast cancer, suggesting a lineage-specific pattern.
  • Evidence suggests faulty repair of abasic sites as the cause of these non-coding mutations.

Conclusions:

  • Non-coding AR binding sites are frequently mutated in prostate cancer.
  • These mutations can influence enhancer activity and potentially impact carcinogenesis and tumor progression.
  • The findings highlight the importance of non-coding DNA mutations in cancer development.

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