论文部分内容阅读
肿瘤细胞DNA甲基化紊乱常表现为癌基因去甲基化和抑癌基因高甲基化,即抑癌基因功能失活是通过表观遗传调控抑制,而不是通过基因缺失或突变。既往研究在肝细胞癌中p16、SOCS-1、TFPI-2、E-cadherin、RASSF1A和NORE1B等抑癌基因常常表现为高甲基化状态,这些基因的高甲基化状态与肝细胞癌的发生、发展关系密切。
Deregulation of DNA methylation in tumor cells is often characterized by demethylation of oncogenes and hypermethylation of tumor suppressor genes, ie, the inactivation of tumor suppressor genes is suppressed by epigenetic regulation rather than by gene deletion or mutation. Previous studies in hepatocellular carcinoma p16, SOCS-1, TFPI-2, E-cadherin, RASSF1A and NORE1B and other tumor suppressor genes often show hypermethylation status, the hypermethylation of these genes and the occurrence and development of hepatocellular carcinoma close.