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

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 downstream 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.