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Updated: May 3, 2026

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR
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MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR qPCR

Published on: May 16, 2012

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Androgen receptor and microRNA-21 axis downregulates transforming growth factor beta receptor II (TGFBR2) expression

S Mishra1, J J Deng1, P S Gowda1

  • 1Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, TX, USA.

Oncogene
|September 17, 2013
PubMed

Insights

Prostate cancer cells evade growth control by downregulating TGFβ receptors via miR-21 and androgen receptor (AR) signaling. This axis inhibits TGFβ

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Prostate cancer cells resist growth inhibition by TGFβ by reducing TGFβ receptors.
  • The precise mechanism for TGFβ receptor downregulation in prostate cancer remains unclear.

Purpose of the Study:

  • To elucidate the mechanism by which prostate cancer cells downregulate TGFβ receptors.
  • To investigate the roles of miR-21 and androgen receptor (AR) signaling in this process.

Main Methods:

  • Analysis of TGFβ receptor II (TGFBR2) expression in relation to miR-21 and AR levels in various prostate cell models and human prostate cancers.
  • Manipulation of androgen signaling, AR, and miR-21 expression in vitro and in vivo.
  • Assessment of TGFβ pathway activation, cell growth, migration, and apoptosis.

Main Results:

  • Coordinated action of miR-21 and AR signaling significantly inhibits TGFBR2 expression in prostate cells.
  • miR-21 directly suppresses TGFBR2 by binding to its 3'-UTR, with AR signaling enhancing this effect.
  • Increased miR-21/AR expression correlates with reduced TGFBR2 in primary prostate cancers, forming a positive feedback loop.
  • The miR-21/AR axis attenuates TGFβ signaling, promoting tumor growth by inhibiting Smad2/3 activation, cell growth inhibition, migration, and apoptosis.

Conclusions:

  • The AR and miR-21 axis drives oncogenic effects in prostate tumors by downregulating TGFBR2, thereby suppressing the tumor-inhibitory activity of the TGFβ pathway.
  • Targeting miR-21, alone or with AR, could restore TGFβ's tumor-suppressive functions in prostate cancer.

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