MiR-31 Functions as a Tumor Suppressor in Lung Adenocarcinoma Mainly by Targeting HuR

Clin Lab. 2016;62(4):711-8. doi: 10.7754/clin.lab.2015.150903.

Abstract

Background: Gene expression is widely regulated by miRNAs and RNA binding proteins. In this study, we mainly focused on miR-31 and a RNA binding protein, HuR (Hu antigen R).

Methods: The levels of miR-31 and HuR in lung carcinoma cells and lung cancer tissues were explored using RT-qPCR and western blot, respectively. Luciferase reporter assay was used to determine the target gene of miR-31. Cell apoptosis and migration were studied using flow cytometry and the transwell invasion assay. The down-stream genes of HuR were explored with western blot assay.

Results: miR-31 was decreased in lung carcinoma cells and lung cancer tissues, while the protein level of HuR was increased. HuR was the target gene of miR-31. Inhibition of miR-31 and overexpression of HuR resulted in the upregulation of cyclins A2, B1, D1 and VEGF (vascular endothelial growth factor). Furthermore, overexpression of miR-31 prompted lung cancer cell apoptosis and inhibited cell migration.

Conclusions: Reduction of miR-31 expression enhanced lung cancer proliferation and migration by repressing HuR expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / pathology*
  • Adenocarcinoma of Lung
  • Apoptosis
  • Cell Proliferation
  • ELAV-Like Protein 1 / genetics*
  • Genes, Tumor Suppressor / physiology*
  • Humans
  • Lung Neoplasms / pathology*
  • MicroRNAs / physiology*
  • Neoplasm Invasiveness

Substances

  • ELAV-Like Protein 1
  • ELAVL1 protein, human
  • MIRN31 microRNA, human
  • MicroRNAs