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Archive > Volume 27 Issue 11 > 2020,27(11):1239-1245. DOI:10.3872/j.issn.1007-385X.2020.11.006 Prev Next
Basic Research
miR-497 over-expression inhibits epithelial-mesenchymal transition in lung cancer A549 cells by targeting cyclin E1
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Abstract:
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.
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