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。
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.
出处
《生命科学研究》
CAS
CSCD
北大核心
2014年第4期292-298,共7页
Life Science Research
基金
国家973项目(2010CB833605)
教育部新世纪优秀人才支持计划项目(NCET-10-0790)
中南大学杰青培育项目(2010QYZD006)
国家自然科学基金项目(30801322
81272972)
湖南省自然科学基金项目(10JJ4025)
中南大学贵重仪器设备开放共享基金资助项目
