基因启动子甲基化和化疗耐药  

Methylation of gene promoter and chemorisistance

作　　者：蔡飏[1] 杨新苗[1] 胡夕春[1] 

机构地区：[1]复旦大学附属肿瘤医院化疗科,复旦大学上海医学院肿瘤学系,上海200032

出　　处：《中国癌症杂志》2006年第11期987-990,共4页China Oncology

摘　　要：表观遗传(eprgenetic)和基因突变、易位、缺失等事件同样在化疗耐药的形成中有重要的作用。表观遗传的重要机制之一-基因的甲基化是细胞中必不可少的一种修饰方式,正常人体细胞大约有29000个CpG岛,并以非随机化的方式主要分布于蛋白编码基因的启动子和第一外显子区域。但是肿瘤细胞中基因甲基化状态有所改变,表现为整体甲基化程度降低和局部甲基化程度的增高,而这些改变进而可以影响肿瘤细胞对于化疗药物的敏感性。我们就基因启动子的异常甲基化和化疗耐药之间的关系作一探讨,并对近来一些基因甲基化及其逆转的研究进行简要回顾。Mutation, translocation and loss of some genes have been known to contribute to chemoresistance, epigenetic mechanisms may also play an important role. About 29 000 CpG islands are primarily distributed in the promoter and the first exon regions of protein coding genes in normal cells. However, cancer cells exhibit significant changes in terms of DNA methylation, which can be summarized as global hypomethylation of the genome accompanied by focal hypermethylation. The relationship between aberrant methylation of gene in the promoter and ehemoresistanee was discussed in the review. A brief summary was also introduced with regard to the advances how in reversing aberrant methylation and overcoming ehemoresistanee.

关 键 词：启动子 基因甲基化 化疗耐药 

分 类 号：R73-361[医药卫生—肿瘤]