miR‐210 is induced by hypoxia and regulates neural cell adhesion molecule in prostate cells

Zoe Angel, Seodhna M Lynch, Heather Nesbitt, Michael M. McKenna, CP Walsh, Declan J McKenna

Research output: Contribution to journalArticle

Abstract

Hypoxia in prostate tumours has been associated with disease progression and
metastasis. MicroRNAs are short noncoding RNA molecules that are important in
several cell processes, but their role in hypoxic signalling is still poorly understood.
miR‐210 has been linked with hypoxic mechanisms, but this relationship has been poorly characterised in prostate cancer. In this report, the link between hypoxia and miR‐210 in prostate cancer cells is investigated. Polymerase chain
reaction analysis demonstrates that miR‐210 is induced by hypoxia in prostate
cancer cells using in vitro cell models and an in vivo prostate tumour xenograft
model. Analysis of The Cancer Genome Atlas prostate biopsy datasets shows that miR‐210 is significantly correlated with Gleason grade and other clinical markers of prostate cancer progression. Neural cell adhesion molecule (NCAM) is
identified as a target of miR‐210, providing a biological mechanism whereby
hypoxia‐induced miR‐210 expression can contribute to prostate cancer. This study
provides evidence that miR‐210 is an important regulator of cell response to
hypoxic stress and proposes that its regulation of NCAM may play an important
role in the pathogenesis of prostate cancer.
Original languageEnglish
Pages (from-to)6194-6203
Number of pages10
JournalJournal of Cellular Physiology
Volume235
Issue number9
Early online date24 Jan 2020
DOIs
Publication statusE-pub ahead of print - 24 Jan 2020

Keywords

  • NCAM
  • hypoxia
  • miR-210
  • microRNA
  • prostate cancer

Fingerprint Dive into the research topics of 'miR‐210 is induced by hypoxia and regulates neural cell adhesion molecule in prostate cells'. Together they form a unique fingerprint.

  • Profiles

    No photo of Declan Mc Kenna

    Declan Mc Kenna

    Person: Academic

    Cite this