miR-617在宫颈癌组织中的表达及其对宫颈癌SiHa细胞生物学行为的影响
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摘要
目的:探讨miR-617在宫颈癌组织中的表达及其过表达对宫颈癌SiHa细胞增殖、凋亡、迁移等细胞生物学行为的影响。方法:采用实时定量PCR法检测宫颈鳞癌组织及正常宫颈组织中miR-617表达。宫颈癌SiHa细胞中转染miR-617模拟物使其过表达,采用CCK-8细胞增殖检测试剂盒检测细胞增殖活力,流式细胞术检测细胞凋亡,平板克隆实验检测细胞克隆形成率,划痕实验检测细胞迁移能力,Western blot法检测靶基因C-末端结合蛋白1(Ct BP1)蛋白表达水平。结果:miR-617在宫颈鳞癌组织中表达下调,过表达miR-617可抑制宫颈癌SiHa细胞增殖,促进SiHa细胞凋亡,抑制SiHa细胞的克隆形成能力,抑制细胞的迁移,过表达miR-617可降低CtBP1蛋白表达。结论:miR-617在宫颈鳞癌中表达下调,可抑制SiHa细胞增殖、促进细胞凋亡、抑制克隆形成和迁移,其作用机制可能与CtBP1蛋白下调有关。
Objective: To investigate the expression of miR-617 in cervical cancer and the effects of its overexpression on cell biological behaviors such as proliferation,apoptosis and migration in cervical carcinoma Si Ha cell. Methods: The expressions of miR-617 in cervical cancer and normal tissue were detected by real time RT-PCR,and miR-617 mimics were transfected into SiHa cell to make it overexpression,cell proliferation activity was determined by CCK-8 cell proliferation assay Kit,and cell apoptosis was detected by flow cytometry,flat cell cloning experiments was used toestimate cell colony-forming ability,cell migration were tested by wounding healing assay,and the expression of target genes c-Terminal binding protein 1( CtBP1) protein was determined by Western blot. Results: The expression of miR-617 in cervical cancer was down-regulated,and overexpression of miR-617 could inhibit SiHa cell proliferation,and promote cell apoptosis,and could inhibit SiHa cellclone formation as well as cell migration,overexpression of miR-617 downregulated the expression of protein CtBP1. Conclusion: miR-617 in cervical cancer were down-regulated,and miR-617 can inhibit SiHa cell proliferation,clone formation and migration,and promote cell apoptosis,the mechanism may be relate to the downregulation of protein CtBP1.
Objective: To investigate the expression of miR-617 in cervical cancer and the effects of its overexpression on cell biological behaviors such as proliferation,apoptosis and migration in cervical carcinoma Si Ha cell. Methods: The expressions of miR-617 in cervical cancer and normal tissue were detected by real time RT-PCR,and miR-617 mimics were transfected into SiHa cell to make it overexpression,cell proliferation activity was determined by CCK-8 cell proliferation assay Kit,and cell apoptosis was detected by flow cytometry,flat cell cloning experiments was used toestimate cell colony-forming ability,cell migration were tested by wounding healing assay,and the expression of target genes c-Terminal binding protein 1( CtBP1) protein was determined by Western blot. Results: The expression of miR-617 in cervical cancer was down-regulated,and overexpression of miR-617 could inhibit SiHa cell proliferation,and promote cell apoptosis,and could inhibit SiHa cellclone formation as well as cell migration,overexpression of miR-617 downregulated the expression of protein CtBP1. Conclusion: miR-617 in cervical cancer were down-regulated,and miR-617 can inhibit SiHa cell proliferation,clone formation and migration,and promote cell apoptosis,the mechanism may be relate to the downregulation of protein CtBP1.
引文
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[3]Hummel R,Wang T,Watson DI,et al.Chemotherapy-induced modification of microRNA expression in esophageal cancer[J].Oncol Rep,2011,26(4):1011-1017
[4]王红红,郝敏,赵卫红.微小RNA在宫颈癌中的研究进展[J].国际妇产科学杂志,2014,41(3):252-255
[5]He Y,Lin J,Ding Y,et al.A systematic study on dysregulated microRNAs in cervical cancer development[J].Int J Cancer,2016,138(6):1312-1327
[6]Zhao C,Shen Y,Tao X,et al.Silencing of Ct BP1 suppresses the migration in human glioma cells[J].J Mol Histol,2016,47(3):297-304
[7]王浩.Ct BP1在上皮性卵巢癌组织中表达及意义[J].齐齐哈尔医学院学报,2013,34(15):2201-2202
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[9]李梦妍,王慧,马遇庆.新疆哈萨克族及汉族食管鳞状细胞癌组织中Ct BP1、Cyclin D1的表达及意义[J].新疆医科大学学报,2016,39(1):21-27
[10]李运千,黄承信,曾思恩,等.羧基末端结合蛋白1对肝癌细胞Hep G2增殖的影响[J].肿瘤防治研究,2014,41(5):384-387
[11]Han Y,Bi Y,Bi H,et al.miR-137 suppresses the invasion and procedure of EMT of human breast cancer cell line MCF-7 through targeting Ct BP1[J].Hum Cell,2016,29(1):30-36
[12]Kottawatta KS,So KH,Kodithuwakku SP,et al.MicroRNA-212 regulates the expression of olfactomedin 1 and C-terminal binding protein 1 in human endometrial epithelial cells to enhance spheroid attachment in vitro[J].Biol Reprod,2015,93(5):109