Hsa-mir-182 suppresses lung tumorigenesis through down regulation of RGS17 expression in vitro

Biochem Biophys Res Commun. 2010 May 28;396(2):501-7. doi: 10.1016/j.bbrc.2010.04.127. Epub 2010 Apr 24.

Abstract

Lung cancer is one of the most devastating diseases worldwide. RGS17 is previously shown to be over-expressed in human lung adenocarcinomas and plays an important role in lung tumor growth. Here we have identified a miRNA, has-mir-182, involved in the regulation of RGS17 expression through two conserved sites located in its 3' UTR region. Consistently, endogenous RGS17 expression level is regulated by hsa-mir-182 in human lung cancer cell lines. Similar to the knockdown of RGS17, ectopic expression of hsa-mir-182 significantly inhibits lung cancer cell proliferation and anchorage-independent cell growth, which can be rescued by re-expression of RGS17. Taken together, these data have provided the first evidence of miRNA regulation of RGS17 expression in lung cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3' Untranslated Regions
  • Binding Sites
  • Cell Proliferation
  • Cell Transformation, Neoplastic / genetics*
  • Down-Regulation
  • Gene Expression Regulation, Neoplastic*
  • Gene Knockdown Techniques
  • Humans
  • Lung Neoplasms / genetics*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • RGS Proteins / genetics*

Substances

  • 3' Untranslated Regions
  • MicroRNAs
  • Mirn182 microRNA, human
  • RGS Proteins
  • RGS17 protein, human