miR-154 inhibits prostate cancer cell proliferation by targeting CCND2

Urol Oncol. 2014 Jan;32(1):31.e9-16. doi: 10.1016/j.urolonc.2012.11.013. Epub 2013 Feb 19.

Abstract

Background: Research has shown reduced expression levels of miR-154 in prostate cancer (CaP). However, the function and molecular mechanisms of miR-154 in this cancer type remains unknown.

Objective: The aims of this study were to examine the functional significance of miR-154 in CaP cells and to identify the novel molecular targets regulated by miR-154.

Materials and methods: miR-154 expression significantly decreased in primary CaP samples compared with nonmalignant samples measured by quantitative reverse transcription polymerase chain reaction. Restoration of miR-154 lowered the potential of CaP cell lines to grow and proliferate in vitro evaluated by CCK-8 assay, colony formation assay, and flow cytometry. miR-154 down-regulated the expression of CCND2 by binding to its 3'-untranslated region by luciferase reporter assay.

Conclusions: miR-154 plays a prominent role in CaP proliferation by suppressing CCND2, and it may provide a new approach to the treatment of CaP.

Keywords: CCND2; Prostate cancer; miR-154.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Cell Cycle
  • Cell Enlargement
  • Cell Line, Tumor
  • Cell Proliferation
  • Cyclin D2 / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Male
  • MicroRNAs / physiology*
  • Middle Aged
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / metabolism

Substances

  • CCND2 protein, human
  • Cyclin D2
  • MIRN154 microRNA, human
  • MicroRNAs