MicroRNA-144-3p Suppressed TGF- β1-induced Lung Cancer Cell Invasion and Adhesion via Regulating Src-Akt-Erk Pathway.

This study aimed to study the mechanisms underlying miR-144-3p 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) siRNA 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 down-regulated miR-144-3p and up-regulated 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...
Source: Cell Biology International - Category: Cytology Authors: Tags: Cell Biol Int Source Type: research