摘要
目的 探讨去甲基化药物5-Aza-dc对膀胱癌ScaBer细胞CDH13基因甲基化状态和蛋白表达以及细胞增殖迁移侵袭的影响.方法 以膀胱癌ScaBer细胞为研究对象,分为5-Aza-dc处理组和对照组.应用5-Aza-dc与ScaBer细胞共同孵育后,用MSP检测CDH13基因甲基化状态、western blot检测CDH13的表达水平、MTT法检测细胞增殖、划痕实验检测细胞迁移能力、Transwell法检测细胞侵袭能力.结果 5-Aza-dc与ScaBer细胞共同孵育后CDH13基因甲基化状态得到逆转,与对照组相比CDH13蛋白表达明显增加(P< 0.05);实验组细胞增殖能力下降,迁移和侵袭能力减弱,与对照组相比差异均有统计学意义(P<0.05).结论 5-Aza-dc可逆转CDH13基因的甲基化状态并使其蛋白表达增加,CDH13表达增加后细胞的增殖、迁移和侵袭能力明显减弱,CDH13有可能成为膀胱癌治疗的新的靶点.
Objectives The purpose of this study was to investigate the influence of 5-Aza-dc on the methylation status and protein expression of CDH13 gene in bladder cancer ScaBer cell,as well as on the proliferation,migration and invasion capability.Methods Bladder cancer ScaBer cells was investigated in this study,and divided into 5-Aza-dc treatment group and control group.MSP was used to detect the methylation status of CDH13 gene; western blot was used to detect the protein expression of CDH13,MMT was used to detect cell proliferation,scratch assay was used to detect cell migration and transwell assay was used to detect cell invasion capability.Results The methylation status of CDH13 gene in bladder cancer ScaBer cell was reversed after the treatment of 5-Aza-dc and the protein expression of CDH13 was increased significantly(P 〈 0.05).The cell proliferation,migration and invasion capability was diminished after the treatment of 5-Aza-dc,and the difference was statistically significant compared to control group(P 〈 0.05).Conclusions The methylation status of CDH13 gene can be reversed after the treatment of 5-Aza-dc and the CDH13 protein expression was increased after the reversion of the methylation status of CDH13 gene.The cell proliferation,migration and invasion capability was decreased significantly after the increasing of CDH13 protein expression,and CDH13 gene may be a novel treatment target for bladder cancer.
出处
《国际泌尿系统杂志》
2015年第1期4-8,共5页
International Journal of Urology and Nephrology
基金
江苏大学医学临床科技发展基金项目(编号:JLY201220077)
徐州市医学青年后备人才项日(编号:2014007)
关键词
膀胱肿瘤
基因
甲基化
细胞增殖
Urinary Bladder Neoplasms
Genes
Methylation
Cell Proliferation