MiR-150 promotes gastric cancer proliferation by negatively regulating the pro-apoptotic gene EGR2

Biochem Biophys Res Commun. 2010 Feb 12;392(3):340-5. doi: 10.1016/j.bbrc.2009.12.182. Epub 2010 Jan 11.

Abstract

Accumulating evidence suggests small non-coding RNAs (microRNAs) play important roles in human cancer progression. In the present study, we found miR-150 was overexpressed in gastric cancer cell lines and tissues. Ectopic expression of miR-150 promoted tumorigenesis and proliferation of gastric cancer cells. Luciferase reporter assay demonstrated that EGR2 was a direct target of miR-150. Collectively, our study demonstrated that overexpression of miR-150 in gastric cancer could promote proliferation and growth of cancer cells at least partially through directly targeting the tumor-suppressor EGR2, suggesting a potential strategy for the development of miRNA-based treatment of gastric cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Base Sequence
  • Carcinoma / genetics
  • Carcinoma / pathology*
  • Cell Line, Tumor
  • Cell Proliferation
  • Early Growth Response Protein 2 / genetics*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Mice
  • Mice, Nude
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Molecular Sequence Data
  • Stomach Neoplasms / genetics
  • Stomach Neoplasms / pathology*

Substances

  • EGR2 protein, human
  • Early Growth Response Protein 2
  • MIRN150 microRNA, human
  • MicroRNAs