胃癌p16基因启动子CpG岛甲基化研究
Hypermethylation of CpG island at p16 gene promoter in gastric carcinomas
罗冲 1周永宁 1郭娴 1杨永成1
作者信息
- 1. 兰州大学第一医院消化内科,甘肃,兰州,730000
- 折叠
摘要
目的:探讨p16基因启动子CpG岛甲基化在胃癌中的表达及意义. 方法:采用特异性甲基化PCR(MSP)法检测p16基因启动子CpG岛甲基化水平. 结果:对照组未检测到CpG岛甲基化,胃癌细胞株均检测到CpG岛甲基化,23例(74%)胃癌组织检测到CpG岛甲基化.此外,17例(74%)癌旁组织检测到CpG岛甲基化.胃癌组织p16基因CpG岛甲基化与分化程度及淋巴结转移之间无相关关系(P>0.05). 结论:胃癌广泛存在p16基因启动子CpG岛甲基化,并且可能是胃癌发生的早期分子事件.
Abstract
AIM: To investigate the expression of hypermethylation of CpG island at the pl6 gene promoter in gastric carcinomas and its significance. METHODS: Hypermethylation of CpG island at the p16 gene promoter was determined by methylation-specific polymerase chain reaction (MSP) analysis. RESULTS: CpG-island hypermethylaion was not detected in control biopsy specimens but was identified in human gastric cancer cell lines and 74.1% (23/31) of gastric carcinoma patients. CpG-island hypermethylaion of p16 gene was detected in 17 adjacent gastric tissues (73.9%, 17/23). In primary gastric tumors, no significant association was found between tumor differentiation status and lymph node metastasis and CpG island methylation status of p16 gene (P＞0.05, respectively). CONCLUSION: Hypermethylation of CpG island at the p16 gene promoter is detected commonly in gastric carcinoma. p16 promoter hypermethylation may be involved in the early gastric carcinogenesis process.
关键词
p16/胃癌/甲基化Key words
p16/gastric carcinoma/hypermethylation引用本文复制引用
基金项目
中国科学院西部之光资助项目(中科院文件2005第404号)
出版年
2009
NETL
NSTL
维普
万方数据