miR-3619-5p inhibits prostate cancer cell growth by activating CDKN1A expression

Oncol Rep. 2017 Jan;37(1):241-248. doi: 10.3892/or.2016.5250. Epub 2016 Nov 16.

Abstract

Recent studies have shown that miRNAs have potent abilities to activate gene expression by targeting promoter elements, a phenomenon known as RNA activation (RNAa). In the present study, we identified a new endogenous miR-3619-5p which was decreased in prostate cancer tissues and cells compared to corresponding normal controls. Moreover, overexpression of miR-3619-5p readily induced CDKN1A gene expression by directly targeting the putative site in the promoter. Besides, miR-3619-5p possessed considerable capacity to inhibit prostate cancer DU145 and PC3 cell growth, and downregulate several CDKN1A downstream genes, such as cyclin D1, CDK4 and CDK6. Notably, this antitumor function of miR-3619-5p was mainly achieved by stimulating CDKN1A expression.

MeSH terms

  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Cyclin D1 / genetics
  • Cyclin-Dependent Kinase 4 / genetics
  • Cyclin-Dependent Kinase 6 / genetics
  • Cyclin-Dependent Kinase Inhibitor p21 / genetics*
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • MicroRNAs / genetics*
  • Promoter Regions, Genetic
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / pathology*

Substances

  • CCND1 protein, human
  • CDKN1A protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • MIRN-3619 microRNA, human
  • MicroRNAs
  • Cyclin D1
  • CDK4 protein, human
  • CDK6 protein, human
  • Cyclin-Dependent Kinase 4
  • Cyclin-Dependent Kinase 6