MicroRNA-144-3p suppressed TGF-β1-induced lung cancer cell invasion and adhesion by regulating the Src-Akt-Erk pathway.

Lung cancer remains a leading cause to cancer-related death worldwide. The anti-cancer ability of microRNA-144-3p has been reported in many cancer types. This study focused on the mechanisms underlying miR-144-3p in inhibiting lung cancer. The expression levels of miR-144-3p and steroid receptor coactivator (Src) in different lung cancer cell lines and those in bronchial epithelial cells (16HBE) were compared. miR-144-3p mimic and siSrc were transfected into A549 cells. Under the conditions of transforming growth factor-β1 (TGF-β1). Small interfering transfection or TGF-β1 treatment, cell invasive and adhesive abilities were analyzed by Transwell and cell adhesion assays. miR-144-3p inhibitor and siSrc were co-transfected into A549 cells and the changes in cell invasion and adhesion were detected. The activation of Src-protein kinase B-extracellular-regulated protein kinases (Src-Akt-Erk) pathway was determined using Western blot. The downregulated miR-144-3p and upregulated Src were generally detected in lung cancer cell lines and were the most significant genes in A549 cells. Both miR-144-3p overexpression and Src inhibition could obviously inhibit the invasion and adhesion abilities of A549 cells in the presence or absence of the effects of TGF-β1. The inhibition of Src could block the promotive effects of miR-144-3p inhibitor and TGF-β1 on cell invasion and adhesion. Furthermore, we found that miR-144-3p could negatively regulate the phosphorylation levels of Akt and Erk. Our data indicated the essential role of Src in the mechanisms underlying TGF-β1-induced cell invasion and adhesion of lung cancer, and that miR-144-3p could effectively suppress TGF-β1-induced aggressive lung cancer cells by regulating Src expression.