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目的 探讨LncRNA OIP5-AS1对非小细胞肺癌放射抗拒细胞A549R的放射敏感性影响及作用机制.方法 X射线6Gy照射5次A549细胞建立放射抗拒细胞A549R.qRT-PCR检测A549、A549R细胞OIP5-AS1和miR-34c-5p表达水平.转染OIP5-AS1抑制剂或miR-34c-5p模拟物至A549R细胞,OIP5-AS1过表达质粒至A549细胞.流式细胞仪检测细胞凋亡,克隆形成实验检测细胞放射敏感性,蛋白印记检测p-Chk2和p-ATM蛋白表达水平.双荧光素酶实验验证OIP5-AS1与miR-34c-5p之间关系.结果 与A549细胞比,A549R细胞中OIP5-AS1表达上调(1.97±0.11:1.01±0.05,P＜0.05),miR-34c-5p表达下调(0.43±0.02:1.02±0.06,P＜0.05).沉默OIP5-AS1 +6 Gy组A549R细胞中p-Chk2和p-ATM蛋白水平低于沉默对照+6Gy组(0.43±0.03:1.39±0.15和0.51±0.05:1.21±0.11,P＜0.05),但凋亡率增加[(13.29±1.25)％:(28.47±2.31)％,P＜0.05].过表达OIP5-AS1 +6 Gy组A549细胞中p-Chk2和p-ATM蛋白水平高于过表达对照+6Gy组(1.23±0.13:0.75±0.06和1.08±0.11:0.59±0.04,P＜0.05).抑制miR-34c-5p表达逆转了沉默OIP5-AS1对A549R细胞存活分数影响,增敏比为1.42.OIP5-AS1负调控miR-34c-5p表达.结论 沉默OIP5-AS1通过上调miR-34c-5p表达增强A549R细胞放射敏感性,为放疗提供潜在的靶点.“,”Objective To investigate the effect of LncRNA OIP5-AS1 on radiosensitivity of non-small cell lung cancer (NSCLC) cells and its mechanism.Methods The radiation-resistant cell A549R was established by using A549 cells irradiated by X-ray 6Gy in 5 fractions.The expression levels of OIP5-AS1 and miR-34c-5p in A549 and A549R cells were detected by qRT-PCR.OIP5-AS1 inhibitor or miR-34c-5p mimetic was transfected into A549R cells,or OIP5-AS1 overexpression plasmid was transfected into A549 cells.Cell apoptosis was detected by flow cytometry.Cell radiosensitivity was analyzed by colony formation assay.The expression levels of p-Chk2 and p-ATM proteins were measured by Western blot.Dual luciferase assay was adopted to verify the relationship between OIP5-AS1 and miR-34c-5p.Results Compared with A549 cells,the expression of OIP5-AS1 was significantly up-regulated in A549R cells (1.97±0.11 vs.1.01±0.05,P＜0.05),whereas the expression of miR-34c-5p was remarkably down-regulated (0.43±0.02 vs.1.02±0.06,P＜0.05).The expression levels of p-Chk2 and p-ATM proteins in A549R cells in the silencing OIP5-AS1 +6Gy group were significantly lower (0.43±0.03 vs.1.39±0.15,0.51 ±0.0 5 vs.1.21 ± 0.11,both P＜0.05),whereas the apoptotic rate was significantly higher than those in the silencing control + 6Gy group [(13.29± 1.25)％ vs.(28.47± 2.31)％,P＜0.05)].The expression levels of p-Chk2 and p-ATM proteins in A549 cells in overexpressing OIP5-AS1+6 Gy group were significantly higher than those in overexpression control+6 Gy group (1.23±0.13 vs.0.75±0.06,1.08±0.11 vs.0.59± 0.04,both P＜0.05).Inhibiting miR-34c-5p expression reversed the effect of silencing OIP5-AS1 on survival fraction of A549R cells (SER =1.42).OIP5-AS1 negatively regulated the expression of miR-34c-5p.Conclusion Silencing OIP5-AS1 enhances the radiosensitivity of radiation-resistant A549 cells by up-regulating the expression of miR-34c-5p,providing a potential target for radiotherapy of NSCLC cells.