miR-101-3p Inhibits Invasion and Migration of Non-small Cell Lung Eancer Cells by Targeting EZH2
Objective:To study the biological function and potential mechanism of miR-101-3p in non-small cell lung cancer(NSCLC).Methods:The expression of miR-101-3p in lung adenocarcinoma and normal tissues was analyzed by TCGA database in UALCAN platform,and the difference of survival rate between high expression group and low expression group of miR-101-3p was ana-lyzed by Kaplan-Meier survival analysis.The expression levels of miR-101-3p in NSCLC cell lines A549,H1299,H1975,PC-9 and lung normal epithelial cells BEAS-2B were detected by qRT-PCR.A549 and H1299 cells transfected with miR-101-3p mimic were divided into miR-101-3p mimic group and miR-NC control group.Cell viability was detected by CCK-8,and cell migration and invasion were detected by Transwell.The target genes and binding sites of miR-101-3p were found and analyzed by bioinformatics analysis and luciferase reporter gene.EZH2 was overexpressed in A549 cells.CCK-8 and wound healing assay were used to detect cell viability and migration ability.Results:Low expression of miR-101-3p in lung adenocarcinoma tissues in the TCGA database and its association with poorer survival prognosis.Similarly,compared with BEAS-2B,the expression of miR-101-3p was lower in NSCLC cells(P<0.05).In addition,transfection of miR-101-3p mimic inhibited the proliferation,migration and invasion of A549 and H1299 cells(P<0.05).EZH2 is a target gene of miR-101-3p.The expression level of EZH2 was reduced after transfection of miR-101-3p mimics into cells,and EZH2 overexpression reversed the inhibitory effect of miR-101-3p on cell viability and migration ability in A549 cells(P<0.05).Conclusion:MiR-101-3p may inhibit the proliferation and migration of NSCLC cells by targeting EZH2.