目的：探讨过表达 miR-497 靶向细胞周期蛋白 E1（cyclin E1，CCNE1）对肺癌 A549 细胞上皮间质转化（epithelialmesenchymal transition，EMT）的影响。方法：常规培养人肺癌A549细胞，细胞实验分为正常组（不加干预）、对照组（转染miR497 mimics-NC）、实验组（转染miR-497 mimics）。采用Transwell小室实验、免疫荧光染色、qPCR、Western blotting法分别检测各组细胞迁移和侵袭能力、蛋白间质标志物α-SMA和上皮标志物E-cadherin的表达、miR-497和CCNE1的表达水平，荧光素酶基因基因报告实验验证miR-497和CCNE1的靶向关系。结果：与对照组和正常组相比，实验组A549细胞迁移和侵袭的数量明显减少（均P<0.05），细胞的间质标志物α-SMA的绿色荧光强度明显减弱（[ 36.95±5.81）vs（98.69±2.36）、（97.94±2.63），均P<0.05]，上皮标志物E-cadherin的绿色荧光强度明显增强（[ 388.41±10.93）vs（100.95±6.37）、（102.55±3.18），均P<0.05]，miR-497 的表达明显升高（均P<0.05），CCNE1的表达均明显下降（均P<0.05）。miR-497能够靶向调控CCNE1的表达。结论：在肺癌A549细胞中miR-497能够靶向调控CCNE1的表达，上调miR-497的表达后能明显抑制A549细胞迁移和侵袭能力，影响EMT相关蛋白的表达。

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.