miR-1204靶向调控DEK蛋白对非小细胞肺癌细胞凋亡的影响及作用机制研究  

Effect and mechanism of miR-1204 targeting DEK protein on apoptosis of nonsmall cell lung cancer cells

作　　者：蒋慧[1] 邵乐健 杨树坤 宋瑞[2] JIANG Hui;SHAO Le-Jian;YANG Shu-Kun;SONG Rui(Department of Respiratory Medicine,Wanbei Coal-Electricity Group General Hospital,Suzhou 234000,China)

机构地区：[1]皖北煤电集团总医院呼吸内科,宿州234000 [2]皖北煤电集团总医院病理科,宿州234000

出　　处：《中国免疫学杂志》2021年第14期1722-1726,共5页Chinese Journal of Immunology

摘　　要：目的:探究miR-1204靶向调控DEK蛋白对非小细胞肺癌细胞凋亡的影响及作用机制。方法:培养人非小细胞肺癌细胞株,采用慢病毒载体构建空白组、miR-1204下调组和miR-1204上调组。ELISA检测DEK蛋白表达;MTT法检测细胞增殖能力;流式细胞仪术检测细胞周期分布及凋亡率;Transwell检测各组细胞侵袭、迁移能力;Western blot检测细胞凋亡相关蛋白Bak、Bcl-2、caspase-9表达。结果:miR-1204上调组DEK呈低表达。在24 h、48 h、72 h,miR-1204下调组DEK表达高于空白组,miR-1204上调组DEK表达低于空白组、miR-1204下调组(P<0.05);miR-1204下调组细胞凋亡率低于空白组,miR-1204上调组细胞凋亡率高于空白组、miR-1204下调组(P<0.05)。miR-1204下调组细胞处于G_1期的比例高于空白组,miR-1204上调组细胞处于G_1期的比例低于空白组、miR-1204下调组(P<0.05)。miR-1204上调组侵袭、迁移细胞数少于空白组、miR-1204下调组(P<0.05)。miR-1204下调组细胞Bcl-2、caspase-9蛋白表达高于空白组,Bak蛋白表达低于空白组,miR-1204上调组细胞Bcl-2、caspase-9蛋白表达低于空白组、miR-1204下调组,Bak蛋白表达高于空白组、miR-1204下调组(P<0.05)。结论:miR-1204上调可降低DEK表达,通过调控Bak、Bcl-2、caspase-9表达抑制细胞增殖,阻滞细胞周期分布,促进细胞凋亡。Objective:To investigate effect of miR-1204 targeting DEK protein on apoptosis of non-small cell lung cancer cells and its mechanism.Methods:Human non-small cell lung cancer cell lines were cultured,which were divided into blank group,downregulated miR-1204 group and up-regulated miR-1204 group by lentiviral vector.ELISA to detect DEK protein expression.MTT method to detect cell proliferation.Flow cytometry to detect cell cycle distribution and apoptosis rate.Transwell to detected cell invasion and migration ability of each group.Western blot to detect expressions of apoptosis related proteins Bak,Bcl-2 and caspase-9.Results:Expression of DEK was lower in up-regulated miR-1204 group.Expression of DEK in down-regulated miR-1204 group was higher than that in blank group at 24 h,48 h and 72 h.Expression of DEK in up-regulated miR-1204 group was lower than that in blank group and down-regulated miR-1204 group(P<0.05).Apoptosis rate in down-regulated miR-1204 group was lower than that in blank group,and apoptosis rate in up-regulated miR-1204 group was higher than that in blank group and down-regulated miR-1204 group(P<0.05).Proportion of cells in G1 phase in down-regulated miR-1204 group was higher than that in blank group,and proportion of cells in G1 phase in up-regulated miR-1204 group was lower than that in blank group and down-regulated miR-1204 group(P<0.05).Number of invasion and migration cells in up-regulated miR-1204 group was lower than that in blank group and down-regulated miR-1204 group(P<0.05).Expressions of Bcl-2 and caspase-9 proteins in down-regulated miR-1204 group was higher than that in blank group,while expression of Bak protein in up-regulated miR-1204 group was lower than that in blank group and down-regulated miR-1204 group,and expression of Bak protein was higher than that in blank group and down-regulated miR-1204 group(P<0.05).Conclusion:Up-regulation of miR-1204 can reduce expression of DEK,inhibit cell proliferation,block cell cycle distribution and promote cell apoptosis by regulating e

关 键 词：非小细胞肺癌 细胞凋亡 细胞增殖 

分 类 号：R734.2[医药卫生—肿瘤]