miR-497 over-expression inhibits epithelial-mesenchymal transition in lung cancer A549 cells by targeting cyclin E1.

Objective: To investigate the effects of overexpressed miR-497 targeting cyclin E1 (CCNE1) on epithelial-mesenchymal transition (EMT) in lung cancer A549 cells. Methods: Human lung cancer A549 cells were routinely cultured, and the experimental cells were divided into normal group (without any intervention), control group (transfected with miR-497 mimics-NC), and experiment group (transfected with miR-497 mimics). Transwell chamber experiment, immunofluorescence staining, qPCR, Western blotting were used to detect cell migration and invasion ability, the expressions of protein interstitial marker α-SMA and epithelial marker E-cadherin, and the expressions of miR-497 and CCNE1 in each group of cells, respectively. Dual luciferase reporter gene assay was used to verify the relationship between miR-497 and CCNE1. Results: Compared with the normal group, the number of migrated and invaded cells in the experiment group decreased significantly (all P<0.05), the green fluorescence intensity of the interstitial marker α-SMA of the experimental group cells was significantly weakened [(36.95±5.81) vs (98.69±2.36), (97.94±2.63), all P<0.05], while the green fluorescence intensity of the epithelium marker E-cadherin was significantly enhanced [(388.41±10.93) vs (100.95±6.37), (102.55±3.18), all P<0.05]; in addition, the expression of miR-497 in the cells of the experiment group was significantly increased (all P<0.05), while theexpression of CCNE1 was significantly decreased (all P<0.05). miR-497 could targetedly regulate the expression of CCNE1. Conclusion: In lung cancer A549 cells, miR-497 can targetedly regulate CCNE1 expression. Up-regulating the expression of miR-497 can significantly inhibit the migration and invasion ability of A549 cells and affect the expression of EMT related protein. [ABSTRACT FROM AUTHOR]