This study was carried out to explore the mechanism of LncRNA MALAT-1 as a competing endogenous RNA to regulate miR-124 in epithelial–mesenchymal transition and development of non-small-cell lung cancer (NSCLC). NSCLC and adjacent tissues were collected for RT-qPCR. The correlation of MALAT-1 and miR-124 was analyzed by Pearson. MALAT-1 expression was measured in NSCLC A549, NCI-H460, NCI-H529, SK-MES-1 cells, and 16HBE cells. A549 cells were selected for cell transfection experiments after the creation of six groups. Luciferase reporter assay and RNA immunoprecipitation were used to verify the relationship between MALAT-1 and miR-124. Expressions of E-cadherin and vimentin were determined by western blot. Cell variability, apoptosis, invasion, and migration were measured by MTT, FCM, transwell assay, and scratch test. LncRNA MALAT-1 expression was higher in NSCLC tissues than that in adjacent tissues, but a lower expression of miR-124 was detected in the former tissues than in the latter tissues. Compared with 16HBE cells, MALAT-1 was highly expressed in NSCLC tissues. Compared with the blank group, E-cadherin and cell apoptosis were increased, but vimentin, cell variability, cell invasion, and migration ability in the si-MALAT-1 and miR-124 mimics groups were reduced. Compared with the blank group, decreased E-cadherin and cell apoptosis and increased vimentin, cell variability, cell invasion, and migration ability were detected in the oe-MALAT-1 group. The oe-MALAT-1+miR-124 mimics group had increased E-cadherin and cell apoptosis, but decreased vimentin, cell variability, cell invasion, and migration ability in comparison with the oe-MALAT-1 group. By competitively regulating miR-124, MALAT-1 can promote epithelial–mesenchymal transition, thus accelerating the development of NSCLC.
