Overexpressed microRNA-182 promotes proliferation and invasion in prostate cancer PC-3 cells by down-regulating N-myc downstream regulated gene 1 (NDRG1)

PLoS One. 2013 Jul 16;8(7):e68982. doi: 10.1371/journal.pone.0068982. Print 2013.

Abstract

MicroRNAs, non-coding 20-22 nucleotide single-stranded RNAs, result in translational repression or degradation and gene silencing of their target genes, and significantly contribute to the regulation of gene expression. In the current study, we report that miR-182 expression was significantly upregulated in prostate cancer tissues and four cell lines, compared to benign prostatic hyperplasia tissues and normal prostatic epithelial (RWPE-1) cells. Ectopic overexpression of miR-182 significantly promotes the proliferation, increases the invasion, promotes the G1/S cell cycle transition and reduces early apotosis of PC-3 cells, while suppression of miR-182 decreased the proliferation and invasion, inhibits the G1/S cell cycle transition and increase early apotosis of PC-3 cells. Additionally, we demonstrated that miR-182 could downregulate expression of NDRG1 by directly targeting the NDRG1 3'-untranslated region. In conclusion, our results suggest that miR-182 plays an important role in the proliferation of human prostate cancer cells by directly suppressing the tumor supressor gene NDRG1. We uncovered a new epigenetic regulation of NDRG1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Cell Cycle Proteins / genetics
  • Cell Cycle Proteins / metabolism*
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Movement / physiology
  • Cell Proliferation
  • Down-Regulation / genetics
  • Down-Regulation / physiology
  • Gene Expression Regulation, Neoplastic / physiology
  • Humans
  • In Vitro Techniques
  • Intracellular Signaling Peptides and Proteins / genetics
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • Male
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • Cell Cycle Proteins
  • Intracellular Signaling Peptides and Proteins
  • MicroRNAs
  • Mirn182 microRNA, human
  • N-myc downstream-regulated gene 1 protein

Grants and funding

This study was supported by grants from National Natural Science Foundation of China (No:30800226), Tianjin Municipal Science and Technology Commission (No:12ZCDZSY17200) and the Second Hospital of Tianjin Medical University (No:y1003). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.