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Updated: May 11, 2026

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
11:29

miRNA Expression Analyses in Prostate Cancer Clinical Tissues

Published on: September 8, 2015

Constitutively active androgen receptor variants upregulate expression of mesenchymal markers in prostate cancer

Félicie Cottard1, Irène Asmane, Eva Erdmann

  • 1INSERM U1113, Fédération de Médecine Translationnelle de Strasbourg (FMTS), Université de Strasbourg, Strasbourg, France.

Plos One
|May 10, 2013
PubMed

Insights

Constitutively active androgen receptor (AR) variants promote prostate cancer progression by increasing N-cadherin and other mesenchymal markers. This finding offers new insights into castration-resistant prostate cancer (CRPC) therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The androgen receptor (AR) signaling pathway is a key therapeutic target for castration-resistant prostate cancer (CRPC).
  • Constitutively active AR variants, lacking the carboxy-terminal region, are implicated in CRPC and may drive tumor progression despite androgen depletion.
  • The precise mechanisms by which these AR variants promote cancer progression remain unclear.

Purpose of the Study:

  • To investigate the impact of constitutively active AR variants on the expression of tumor progression markers in prostate cancer.
  • To elucidate the role of these variants in the context of castration-resistant prostate cancer.

Main Methods:

  • Overexpression of wild-type AR and constitutively active AR variants in LNCaP and C4-2B prostate cancer cell lines.
  • Analysis of N-cadherin, Vimentin, SNAIL, and ZEB1 expression using qRT-PCR, Western blot, and immunofluorescence.

Main Results:

  • Constitutively active AR variants significantly increased N-cadherin expression in prostate cancer cells.
  • Upregulation of other mesenchymal markers, including VIMENTIN, SNAIL, and ZEB1, was observed in the presence of these AR variants.
  • Downregulation of E-cadherin was not observed, despite the increase in N-cadherin.

Conclusions:

  • Constitutively active AR variants play a significant role in regulating mesenchymal markers, suggesting a novel mechanism for prostate cancer progression.
  • These findings highlight potential new therapeutic strategies targeting AR variants in CRPC.

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