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5-Aza-CdR对人食管癌细胞株中T-cadherin基因表达和细胞增殖的影响
Effect of 5-Aza-CdR on Expression of T-cadherin Gene and Cell Proliferation in Human Esophageal Carcinoma Cell Line
【摘要】 背景:T-cadherin在肿瘤的发生中可能扮演肿瘤抑制基因的角色,在食管癌等多种肿瘤中的表达明显下降。目的:探讨去甲基化制剂5.氮杂.2’.脱氧胞苷(5.Aza.CdR)对人食管癌细胞株EC109中T-cadherin基因表达和细胞增殖的影响。方法:常规培养人食管癌细胞株EC109,并分为5μmol/L.5.Aza.CdR组和对照组。以甲基化特异性PCR(MSP)法检测T-cadherin基因启动子区甲基化状态,RT.PCR和蛋白质印迹法分别检测T-cadherin mRNA和蛋白表达.MTT法检测EC109细胞增殖。结果:对照组EC109细胞中T-cadherin基因启动子区呈异常甲基化状态,5-Aza-CdR干预可逆转甲基化状态。与对照组相比.5.Aza.CdR组T-cadherin基因mRNA和蛋白表达均显著增高(P<0.01),细胞增殖明显受到抑制。结论:去甲基化制剂5.Aza.CdR通过逆转食管癌细胞中T.cadherin基因启动子区甲基化状态来增强其表达,并抑制肿瘤细胞增殖。
【Abstract】 Background:T-cadherin may function as a tumor suppressor gene in the process of tumorigenesis,and down-regulation of T-cadherin in various human cancers has been reported,including esophageal carcinoma.Aims:To investigate the effect of demethylating agent 5-azacytidine-2’-deoxycytidines(5-Aza-CdR)on expression of T-cadherin gene and cell proliferation in human esophageal carcinoma cell line EC109.Methods:Human esophageal carcinoma cell line EC109 was cultured conventionally and divided into 5μmol/L 5-Aza-CdR treatment group and control group. Methylation-specific PCR(MSP)was used to detect the methylation of T-cadherin gene promoter.RT-PCR and Western blotting were used to assess expressions of T-cadherin mRNA and protein,respectively.Proliferation of EC109 cells was measured by MTT assay.Results:T-cadherin gene promoter was hypermethylated in control EC109 cells,and the methylation was reversed after treatment with 5-Aza-CdR.Expressions of T-cadherin mRNA and protein were significantly increased(P<0.01)and cell proliferation was obviously inhibited in 5-Aza-CdR treatment group than in control group. Conclusions:Demethylating agent 5-Aza-CdR can effectively increase the expression of T-cadherin by reversing the promoter hypermethylation in human esophageal carcinoma cells,and inhibit the cell proliferation.
【Key words】 5-Azacytidine-2’-Deoxycytidines; Cadherins; Esophageal Neoplasms; Methylation;
- 【文献出处】 胃肠病学 ,Chinese Journal of Gastroenterology , 编辑部邮箱 ,2011年05期
- 【分类号】R735.1
- 【被引频次】2
- 【下载频次】74