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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。
Deletion of liver cancer-1 (DLC-1) in a variety of tumors showed loss of expression or downregulation, this abnormal expression mainly by DNA methyltransferases (DNA methyltransferases, DNMTs) involved in the start Sub-region abnormal methylation. The results of RT-PCR showed that the expression level of DLC-1 in immortal nasopharyngeal epithelial cells NP69 and DNMTs 5-8F cells was significantly higher than that in non-interfering nasopharyngeal carcinoma cells. The result of methylation-specific PCR (MSPCR) showed that the DLC-1 promoter region was abnormally hypermethylated in nasopharyngeal carcinoma cells with downregulation or deletion of DLC-1, while DLC -1 promoter region methylation status was reversed, of which DNMT1 specific interference effect was slightly significant, suggesting that DNA methyltransferase activity of nasopharyngeal carcinoma DLC-1 promoter methylation has an important regulatory role, The role of DNMT1 regulation is more prominent.