Suppression of proliferation, migration and invasion in non-small cell lung cancer cells via profilin 2 inhibition by microRNA-194

Abstract

Purpose: To investigate the anti-tumor effect of microRNA-194 (miR-194) and possible relationship with profilin 2. Methods: The expressions of miR-194 and profilin 2 were investigated via bioinformatic analysis and were further verified using quantitative real-time polymerase chain reaction (qRT-PCR) in both normal and non-small cell lung cancer (NSCLC) cells. Dual luciferase reporter assay, together with transfection, was applied to determine the effect of miR-194 and profilin 2 on proliferation, migration and invasion, and its underlying mechanisms. Results: Relatively low expression of miR-194 and high expression of profilin 2 in cancerous lung tissue were found through bioinformatic analysis and further confirmed by qRT-PCR on normal and NSCLC cell lines. Profilin 2 was the direct target of miR-194. Also, miR-194 overexpression inhibited the proliferation, migration and invasion of NSCLC cells, and this suppressive effect was partially reversed by transfection of pcDNA3.1-PFN2 plasmid. Conclusion: The results show that miR-194 plays a tumor suppressor role in NSCLC development. It inhibits the proliferation, migration and invasion of NSCLC cells via profilin 2 suppression. Interventions targeting the miR-194/profilin 2 axis may therefore serve as a clinical strategy for the prevention and treatment of NSCLC metastases.

MiR-10b alleviates high glucose-induced human retinal endothelial cell injury by regulating TIAM1 signaling

“…Most mature miRNAs precisely regulate target genes by binding to the 3'untranslated region (UTR) of their mRNAs [7]. Compelling evidence has indicated that miRNAs play vital roles in many biological processes, including tumorigenesis, apoptosis, proliferation, and cell differentiation [8][9][10]. For example, miRNA-1273g-3p and miRNA-451a have been shown to play vital roles in the regulation of DR; thus, they may serve as new targets for DR treatment [11,12].…”