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Activated androgen receptor downregulates E-cadherin gene expression and promotes tumor metastasis

Yan-Nian Liu1, Ying Liu, Han-Jung Lee

  • 1Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.

Molecular and Cellular Biology
|September 17, 2008
PubMed

Insights

Activated androgen receptor (AR) represses E-cadherin, promoting tumor metastasis. This mechanism, similar to Snail, offers new therapeutic targets for invasive ductal carcinomas.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Loss of E-cadherin gene expression disrupts cell-cell junctions, promoting tumor metastasis.
  • Snail family transcription factors are known repressors of E-cadherin expression.

Purpose of the Study:

  • To investigate the role of the activated androgen receptor (AR) as a novel repressor of E-cadherin gene expression.
  • To determine if AR activation promotes tumor metastasis.

Main Methods:

  • In vitro and in vivo binding assays of activated AR to the E-cadherin promoter.
  • Assessment of synergistic effects of AR and HDAC1 on E-cadherin expression.
  • Cell morphology analysis after dihydrotestosterone (DHT) treatment.
  • In vivo metastasis assays using breast cancer cells and DHT treatment.
  • Analysis of clinical breast cancer patient data for AR and E-cadherin expression levels.

Main Results:

  • Activated AR binds to the E-cadherin promoter.
  • AR and HDAC1 synergistically downregulate E-cadherin expression.
  • DHT treatment reduces E-cadherin expression, inducing epithelial-to-mesenchymal transition (EMT).
  • DHT treatment promotes metastasis of AR-expressing breast cancer cells in vivo.
  • Clinical data show high nuclear AR and low E-cadherin levels in invasive ductal carcinomas.

Conclusions:

  • Activated androgen receptor (AR) is a novel repressor of E-cadherin, promoting tumor metastasis.
  • AR-mediated E-cadherin downregulation contributes to epithelial-mesenchymal transition (EMT) and metastasis.
  • AR represents a potential therapeutic target for preventing metastasis in breast cancer.

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