中文摘要：

肝癌缺失基因-1（deleted in liver cancer-1,DLC-1）在多种肿瘤中呈现表达缺失或表达下调,这种异常表达主要与由DNA甲基转移酶（DNA methyltransferases,DNMTs）参与的启动子区异常甲基化有关。RT-PCR结果显示DLC-1在永生化鼻咽上皮细胞NP69和干扰DNMTs的5-8F细胞中的表达水平较未干扰的鼻咽癌细胞明显升高。甲基化特异性PCR（methylation-specific PCR,MSPCR）结果则表明DLC-1启动子区在表达下调或缺失的鼻咽癌细胞中均存在异常高甲基化,而干扰DNMTs后5-8F细胞中DLC-1启动子区甲基化状态被逆转,其中特异性干扰DNMT1后效果略为显著,提示DNA甲基转移酶活性对于鼻咽癌中DLC-1启动子区甲基化水平具有重要的调控作用,而DNMT1的调控作用更为突出。

英文摘要：

Deleted in liver cancer-1（DLC-1） shows loss of expression or down-regulation of expression in a variety of tumors because of promoter hypermethylation with DNA methyltransferases（DNMTs）. RT-PCR results showed DLC-1 expression were higher in control nasopharyngeal cell line NP69 and 5-8F cells which was knockdown of DNMT1, DNMT3 A and DNMT3 B than all 7 NPC cell lines. The promoter hypermethylation of DLC-1 was detected in all 7 NPC cell lines but the DLC-1 promoter could be partially demethylated in 5-8F cells with knockdown of DNMTs, especially DNMT1 with more signifecant effect. Thus, our data suggested that DNMTs, esp. DNMT1, might play important roles in methylation maintenance of DLC-1 in NPC.