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Updated: May 23, 2026

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
11:29

miRNA Expression Analyses in Prostate Cancer Clinical Tissues

Published on: September 8, 2015

Androgen-regulated processing of the oncomir miR-27a, which targets Prohibitin in prostate cancer

Claire E Fletcher1, D Alwyn Dart, Ailsa Sita-Lumsden

  • 1Androgen Signalling Laboratory, Department of Surgery and Cancer, Imperial College London, London W12 0NN, UK.

Human Molecular Genetics
|April 17, 2012
PubMed

Insights

MicroRNAs (miRs) are key in disease. In prostate cancer, miR-27a promotes tumor growth by targeting Prohibitin (PHB), offering a potential therapeutic target.

Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • MicroRNAs (miRs) are crucial regulators in human diseases, exhibiting either tumor suppressor or oncogenic (oncomir) functions.
  • Prostate cancer is initially driven by androgens, with the androgen receptor (AR) continuing to drive growth in castration-resistant tumors.
  • The specific AR-mediated oncomiR pathways in prostate cancer require further elucidation.

Purpose of the Study:

  • To investigate the role of miR-27a in prostate cancer.
  • To elucidate the mechanisms of androgen-mediated regulation of oncomiRs.
  • To explore the therapeutic potential of targeting miR-27a in prostate cancer.

Main Methods:

  • Investigated miR-27a expression and its target Prohibitin (PHB) in prostate cancer cells.
  • Analyzed the impact of miR-27a on AR target gene expression and cell growth.
  • Examined androgen-mediated regulation of miR-23a27a24-2 cluster transcription and processing.
  • Assessed the therapeutic efficacy of a miR-27a anti-sense oligonucleotide.

Main Results:

  • miR-27a was identified as an androgen-regulated oncomiR in prostate cancer.
  • Increased miR-27a reduced PHB levels and enhanced AR target gene expression and prostate cancer cell proliferation.
  • Androgen receptor (AR) regulates miR-27a via both transcriptional activation of the miR-23a27a24-2 cluster and accelerated processing of the primary miRNA.
  • A miR-27a anti-sense oligonucleotide demonstrated therapeutic potential by counteracting miR-27a effects.

Conclusions:

  • miR-27a acts as an oncomiR in prostate cancer by targeting the tumor suppressor Prohibitin (PHB).
  • Androgens employ a dual mechanism (transcriptional and post-transcriptional) to upregulate miR-27a.
  • Targeting miR-27a with anti-sense oligonucleotides presents a promising therapeutic strategy for prostate cancer.

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