MicroRNA-198 inhibits proliferation and induces apoptosis of lung cancer cells via targeting FGFR1

J Cell Biochem. 2014 May;115(5):987-95. doi: 10.1002/jcb.24742.

Abstract

Lung cancer is the most common cause of death from cancer worldwide and recent studies have revealed that microRNAs play critical roles to regulate lung carcinogenesis. Here we present evidence to show the role of miR-198 in lung cancer development. Our results showed that ectopic expression of miR-198 inhibits the viability and induces the apoptosis of human non-small cell lung cancer cells A549 and NCI-H460, while miR-198 inhibition resulted in opposite changes. In nude mice miR-198 inhibits A549 growth of tumor graft. We further demonstrated that miR-198 directly targets fibroblast growth factor receptor 1 (FGFR1) in lung cancer cells. Restoring FGFR1 expression blocked the inhibitory function of miR-198, while FGFR1 inhibition achieved the similar phenotypes of miR-198 overexpression. Hence, our data delineates the molecular pathway by which miR-198 inhibits lung cancer cellular proliferation and induces apoptosis, and may have important implication for the treatment of lung carcinogenesis.

Keywords: APOPTOSIS; FGFR1; LUNG CARCINOGENESIS; VIABILITY; miR-198.

Publication types

  • Retracted Publication

MeSH terms

  • Animals
  • Apoptosis / genetics
  • Carcinoma, Non-Small-Cell Lung / genetics*
  • Carcinoma, Non-Small-Cell Lung / pathology
  • Cell Line, Tumor
  • Cell Proliferation
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / pathology
  • Mice
  • MicroRNAs / genetics*
  • Receptor, Fibroblast Growth Factor, Type 1 / genetics
  • Receptor, Fibroblast Growth Factor, Type 1 / metabolism*
  • Signal Transduction / genetics
  • Xenograft Model Antitumor Assays

Substances

  • MIRN198 microRNA, human
  • MicroRNAs
  • FGFR1 protein, human
  • Receptor, Fibroblast Growth Factor, Type 1