miR-150 promotes the proliferation of lung cancer cells by targeting P53

FEBS Lett. 2013 Aug 2;587(15):2346-51. doi: 10.1016/j.febslet.2013.05.059. Epub 2013 Jun 6.

Abstract

Lung cancer is one of the most common causes for cancer-related death. Previous studies suggested that uncontrolled cell proliferation induced by activation of pro-cancer genes or inhibition of cancer suppressor genes plays an important role in the pathogenesis of lung cancer. Here, we demonstrate that miR-150 is aberrantly upregulated in lung cancer tissue and negatively correlates with the expression of the proapoptotic gene p53 but not EGR2. We show that miR-150 specifically targets the 3'-UTR of p53 and regulates its expression. Inhibition of miR-150 effectively delays cell proliferation and promotes apoptosis, accompanied by increased p53 protein expression. Our data reveals the mechanisms underlying miR-150 regulated lung cancer pathogenesis, which might be beneficial for lung cancer therapy.

Keywords: Cell proliferation; Lung cancer; P53; miR-150.

MeSH terms

  • Base Sequence
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / pathology*
  • Cell Proliferation*
  • DNA Primers
  • Humans
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology*
  • MicroRNAs / physiology*
  • Tumor Suppressor Protein p53 / physiology*

Substances

  • DNA Primers
  • MIRN150 microRNA, human
  • MicroRNAs
  • Tumor Suppressor Protein p53