miR-181a-3p from Exosome Excreted by BMSCs Promotes Apoptosis of Lung Cancer Cells Through Activating PR-ERAD Signal Pathway

Our study aimed to assess the effect of miR-181a-3p from exosome excreted by BMSCs on lung cancer cell apoptosis. Lung cancer cells A549 and normal pulmonary epithelial cells were cultivated in vitro to measure ERAD and PR mRNA level by qRT-PCR or Western blot assay along with analysis of cell proliferative activity by CCK-8, apoptosis by flow cytometry and level of ERAD, PR and p-AKT. ERAD in A549 cells was significantly elevated compared with BEAS-2B cells and PR was reduced. A549 cell proliferation was restrained after treated with miR-181a-3p from exosome excreted by BMSCs and cell apoptosis was promoted in a dose-dependent manner. ERAD was down-regulated and PR was up-regulated by miR-181a-3p from exosome excreted by BMSCs in varied concentrations. The proliferation and cell growth of lung cancer could be restrained by exosome derived from BMSCs through restraining the proliferative signal pathway. The activity of PR-ERAD was affected by the miR-181a-3p from exosome excreted by BMSCs, leading to inhibited proliferation and promoted apoptosis of lung cancer cells.