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MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR (qPCR)
08:30

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

Published on: May 16, 2012

miR-141 modulates androgen receptor transcriptional activity in human prostate cancer cells through targeting the

Jing Xiao1, Ai-Yu Gong, Alex N Eischeid

  • 1Department of Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, Nebraska 68178, USA.

The Prostate
|February 9, 2012
PubMed
Abstract

Insights

MicroRNA-141 (miR-141) upregulation downregulates small heterodimer partner (Shp) in prostate cancer (PCa) cells, promoting cancer growth. Shp and miR-141 are potential targets for PCa chemoprevention.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • Aberrant microRNA expression, including miR-141 upregulation, is linked to prostate cancer (PCa) tumorigenesis.
  • Small heterodimer partner (Shp) acts as a co-repressor for the androgen receptor (AR), inhibiting AR-regulated transcription.

Purpose of the Study:

  • To investigate the relationship between Shp expression and miR-141 levels in prostate cells.
  • To determine the impact of this interaction on androgen receptor transcriptional activity.

Main Methods:

  • Analysis of Shp and miR-141 expression in non-malignant and malignant human prostate cell lines.
  • Investigation of miR-141 targeting of Shp mRNA and its effect on AR activity.
  • Utilizing enforced Shp expression and miR-141 inhibition (anti-miR-141) in LNCaP cells.
  • Assessing the effects of phenethyl isothiocyanate on Shp, miR-141, and AR activity.

Main Results:

  • Shp was downregulated, while mature miR-141 was upregulated in PCa cell lines.
  • miR-141 directly targets Shp mRNA, leading to translational suppression and degradation.
  • Enforced Shp expression or miR-141 inhibition reduced AR transcriptional activity.
  • Phenethyl isothiocyanate increased Shp, decreased miR-141, and inhibited AR activity in LNCaP cells.

Conclusions:

  • Shp is a direct target of miR-141, and its downregulation in PCa cells is associated with miR-141 upregulation.
  • This interaction promotes AR transcriptional activity, contributing to prostate cancer progression.
  • Shp and miR-141 represent potential therapeutic targets for prostate cancer chemoprevention.

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