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作 者:陈民彪[1] 蔡仁中[1] 黄明芳[1] 黄修明[1] 廖绪强[1] CHEN Minbiao;CAI Renzhong;HUANG Mingfang;HUANG Xiuming;LIAO Xuqiang(Hainan Hospital Affiliated to Hainan Medical College, Hainan Provincial People's Hospital, Haikou 570311, China)
机构地区:[1]海南省人民医院·海南医学院附属海南医院胸外科,海南海口570311
出 处:《西部医学》2022年第1期16-20,共5页Medical Journal of West China
基 金:海南省卫生计生行业科研项目(18A200050)。
摘 要:目的探讨AS-miR-16-5p对非小细胞肺癌(NSCLC)A549细胞活性和迁移能力的影响及潜在的作用机制。方法将NSCLC A549细胞分为3组,分别为Black组、miR-NC组和AS-miR-16-5p组。miR-NC组和AS-miR-16-5p组分别转染阴性对照miRNA(miR-NC)及AS-miR-16-5p,Black组不进行任何干预。通过实时定量聚合酶链反应(RT-qPCR)检测A549细胞中miR-16-5p的表达;应用MTT检测A549细胞活性;划痕实验和Transwell实验检测A549细胞迁移能力;Western blotting法检测A549细胞中PTEN/PI3K/AKT信号通路关键蛋白表达水平。结果与miR-NC组和Black组相比,AS-miR-16-5p组miR-16-5p表达水平下调(P<0.05);AS-miR-16-5p显著抑制A549细胞活性,显著减少A549细胞迁移率(均P<0.05);AS-miR-16-5p显著上调A549细胞中PTEN蛋白表达水平,而显著下调PI3K和AKT蛋白表达水平(P<0.05)。结论AS-miR-16-5p能抑制NSCLC A549细胞活性和迁移能力,此外,AS-miR-16-5p通过负调控PTEN/PI3K/AKT信号通路有可能成为NSCLC治疗新靶点。Objective To investigate the effect of AS-miR-16-5p on the cell viability and migration of non-small cell lung cancer(NSCLC)A549 cells and its potential mechanism.Methods NSCLC A549 cells were divided into black group,Mir NC group and AS Mir 165p group.Mir NC group and AS Mir 165p group were transfected with negative control miRNA(MIR NC)and AS Mir 165p respectively.Black group did not intervene.The expression of Mir 165p in A549 cells was detected by real-time quantitative polymerase chain reaction(RT qPCR).MTT assay was used to detect the activity of A549 cells.The migration ability of A549 cells was detected by scratch test and Transwell test.The expression of key proteins of PTEN/PI3K/Akt signaling pathway in A549 cells was detected by Western blotting.Results Compared with the miR-NC group and the Black group,the expression level of miR-16-5p in the AS-miR-16-5p group was down-regulated(P<0.05).AS-miR-16-5p significantly inhibited the viabilit of A549 cells(P<0.05),significantly reduce the migration rate(P<0.05)of A549 cells.AS-miR-16-5p significantly increased the expression level of PTEN protein in A549 cells(P<0.05),and significantly down-regulated the expression of PI3K and AKT protein(P<0.05).Conclusion AS-miR-16-5p can inhibit the cell viability and migration of NSCLC A549 cells.In addition,AS-miR-16-5p negatively regulates the PTEN/PI3K/AKT signaling pathway and may become a new target for NSCLC therapy.
关 键 词:miR-16-5p 非小细胞肺癌 PTEN/PI3K/AKT信号通路 细胞活性 迁移
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