Objective:To investigate the effect and mechanism of miR-126-3 p on the migration and invasion of lung adeno-carcinoma cells.Methods:Predict downstream target genes of miR-126-3p via database and perform enrichment analysis on them.Lung adenocarcinoma cells PC9 and A549 were cultured,and miR-126-3p inhibitor,pcDNA3.1-BCL and si-BCL2 were transfected into A549 and PC9 cells,which were divided into miR-126-3p inhibitor group and inhibitor NC group,pcDNA3.1-BCL2 and pcDNA3.1 groups,miR-126-3p inhibitor+si-BCL2 groups.RT-QPCR detectes the mRNA expression levels,and Western blot detectes the protein expression.Scratch assay and Transwell assay detecte the migration and invasion ability of PC9 and A549 cells.The binding of miR-126-3p to BCL2 was confirmed by dual luciferase reporter Gene Assay.Results:BCL2 was a target gene of miR-126-3p,and enrichment analysis results revealed key functions and pathways related to cell migration and invasion.RT-qPCR showed that miR-126-3p was overexpressed in PC9 and A549 cells compared to normal lung epithelial cells(P＜0.05),while BCL2 was underexpressed in PC9 and A549 cells compared to normal lung epithelial cells,and the ex-pression level of BCL2 was increased after inhibition of miR-126-3p(P＜0.05).Scratch assay and Transwell assay showed that the migration rate and invasion rate of miR-126-3p inhibitor group were lower than those of inhibitor NC group(P＜0.05).The mobility and invasion rate of pcDNA3.1-BCL2 group were lower than those of pcDNA3.1 group(P＜0.05).The migra-tion rate and invasion rate of miR-126-3p inhibitor+si-BCL2 group were higher than those of miR-126-3p inhibitor group(P＜0.05).Western blot analysis of BCL2 protein showed that the histone of miR-126-3p inhibitor was higher than that of inhibitor NC group(P＜0.05),and the histone of miR-126-3p inhibitor+si-BCL2 was lower than that of miR-126-3p inhibitor group(P＜0.05).Conclusion:miR-126-3p promotes the migration and invasion of Lung adenocarcinoma cells by targeting BCL2.