Abstract:ObjectiveTo investigate the expression of microRNA-30 (miR-30) in human non-small cell lung cancer (NSCLC) and its effect on proliferation,migration and erlotinib resistance of lung cancer cells. Methods Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to quantify the expression level of miR-30 in 30 pairs of NSCLC tissues and adjacent tissues,and the expression level of miR-30 in lung cancer cell lines PC9 and PC9G (TKI resistant strains),and to calculate the difference of expression.The miR-30 overexpression reagents were transfected into PC9G cells,and inhibitors of miR-30 were transfected into PC9 cells.Negative control groups were set up respectively.The transfection efficiency was detected by qRT-PCR.CCK-8 kit was used to detect cell proliferation activity,clone formation test,Transwell invasion test and flow cytometry to determine the effects of miR-30 on cell growth,invasion and apoptosis.Luciferase reporter gene detection and Western blot confirmed that SMAD2 may be the target gene of miR-30. Results The expression of miR-30 in non-small cell lung cancer was significantly lower than that in adjacent tissues (P<0.05).In PC9-resistant strain PC9G,the expression of miR-30 was significantly lower than that in PC9 cells (P<0.01).Overexpression of miR-30 in PC9G cells could reduce cell proliferation and migration and reverse cell resistance to erlotinib.Inhibiting the expression of miR-30 in PC9 cells can significantly increase the proliferation and migration ability of PC9 cells,and endow them with resistance to erlotinib.SMAD2 was the target gene of microRNA-30,which played an important role in the development of lung cancer. Conclusion Overexpression of miR-30 can inhibit the proliferation and migration of PC9G cells and reverse their resistance to erlotinib.