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目的:探讨微小RNA(miRNA，miR)-96通过靶向叉头框转录因子O1(FOXO1)促进肺癌细胞增殖和迁移的作用。方法:应用茎环反转录荧光定量聚合酶链反应(RT-qPCR)法检测miR-96在肺癌细胞株中的表达；干扰慢病毒感染抑制miR-96表达后，分别利用细胞增殖试验(CCK-8)和划痕试验检测其对肺癌细胞增殖和迁移的影响；蛋白质印迹法(Western blot)和双荧光素酶活性试验验证miR-96靶基因FOXO1。应用GraphPad Prism 5统计学软件进行分析，计量资料比较采用n t检验。n 结果:CCK-8实验显示抑制H1299细胞miR-96表达后，实验组24、48、72 h吸光度值分别为1.293±0.019、1.684±0.038、2.180±0.034，明显低于对照组的1.655±0.056、1.880±0.020、2.493±0.060，差异有统计学意义(n t＝5.646、4.426、14.670，n P<0.01)；划痕试验显示对照组4 h和10 h细胞迁移率为(29.21±3.96)%、(47.49±3.33)%，明显高于实验组[(5.80±2.94)%、(13.63±3.18)%]，差异有统计学意义(n t＝4.748、7.352，n P<0.01)；筛选miR-96靶基因FOXO1，将miR-96过表达后，肺癌细胞FOXO1表达明显降低；反之，抑制miR-96表达后，FOXO1表达明显增高。荧光素酶活性试验显示miR-96和FOXO1 3’非翻译区(3’UTR)野生型质粒共转染后，野生型为(22.5±7.6)%，与对照组的(97.2±13.2)%及突变型的(115.6±13.5)%比较，荧火虫/海肾荧光素酶比值明显降低(n t＝14.750、12.040，n P值均<0.01)。n 结论:miR-96通过靶向调控FOXO1促进肺癌细胞增殖和迁移。“,”Objective:To investigate the role of microRNA (miRNA, miR) -96 in promoting the proliferation and migration of lung cancer cells by targeting forkhead box O1 (FOXO1).Methods:The miR-96 expression in lung cancer cell lines was detected by stem-loop reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Silencing lentiviral miR-96 was used to infect with lung cancer cells and then the proliferation and migration ability of lung cancer cells was evaluated by cell counting kit (CCK) -8 assay and scratch test, respectively. Western blotting and dual luciferase activity assays was utilized to validate the target gene FOXO1 of miR-96. GraphPad Prism 5 statistical software was used, and the t-test was adopted to compare the difference of the measurement data.Results:CCK-8 assay showed that after inhibiting the expression of miR-96 in H1299 cells, the optical density (OD) at 24, 48 and 72 h was 1.293±0.019, 1.684±0.038, and 2.180±0.034, which was lower than the controls of 1.655±0.056, 1.880±0.020, and 2.493±0.060 (n t=5.646, 4.426, and 14.670, n P<0.01, 0.01, and 0.01, respectively). Moreover, the scratch test showed that the cell migration rate of controls was (29.21±3.96)% and (47.49±3.33)%, higher than in the experimental group of (5.80±2.94)% and (13.63±3.18)% (n t=4.748, 7.352, n P<0.01, 0.01, respectively). We screened the target gene of miR-96 and found that upregulation of miR-96 significantly downregulated the FOXO1 expression in lung cancer cells. In contrast, FOXO1 expression was significantly increased after inhibition of miR-96 expression. Luciferase activity assay revealed that co-transfection of miR-96 and FOXO1 3’ untranslated region (3’UTR) wild type plasmid had lower ratio of firefly/renilla luciferase (22.5±7.6)% than co-trasfection with the mutant type plasmid (115.6±13.5)% and controls (97.2±13.2)% (n t=14.750, 12.040, n P all<0.01).n Conclusion:miR-96 promotes the proliferation and migration of lung cancer cells by targeting FOXO1, which might serve as potential diagnosis and therapy target, however, the detailed mechanism should be studied in future.