摘要
CpG岛的高甲基化是肿瘤中作为抑癌基因microRNA失活的重要表观遗传机制之一。利用UCSC预测hsa-miR-24、hsa-miR-126、hsa-miR-132、以及hsa-miR-136定位于CpG岛内部或附近,采用甲基化酶抑制剂5-Aza-CdR处理鼻咽癌细胞5-8f,经RT-PCR与MSP检测,结果表明hsa-miR-136在5-8f中存在高甲基化,5-Aza-CdR能逆转hsa-miR-136甲基化,恢复hsa-miR-136的表达。外源过表达hsa-miR-136能明显抑制鼻咽癌细胞5-8f的增殖;同时流式细胞技术检测显示,hsa-miR-136能诱导5-8f细胞发生晚期凋亡,迁移实验也显示hsa-miR-136能明显抑制5-8f细胞的迁移。综上所述,hsa-miR-136可作为治疗鼻咽癌潜在的靶标。
Hypermethylation of CpG island is one of the important epigenetic mechanisms of tumor suppressor microRNAs inactivation in carcinoma cells.Hsa-miR-24,hsa-miR-126,hsa-miR-132 and hsa-miR-136 were predicted by UCSC to be located in or near CpG islands.Only hsa-miR-136 was confirmed to be hypermethylated in nasopharyneal carcinoma cell 5-8f by using RT-PCR and MSP and expression of hsa-miR-136 could be resumed with 5-Aza-CdR,which is a methylase inhibitor.The proliferation and the metastasis of 5-8f cells were inhibited by overexpression of hsa-miR-136.Result showed that hsa-miR-136 could induce apoptosis of 5-8f cells.
出处
《生物学杂志》
CAS
CSCD
2012年第1期9-12,20,共5页
Journal of Biology
基金
国家自然科学基金(No.81071524)
关键词
hsa-miR-136
鼻咽癌
增殖
迁移
凋亡
hsa-miR-136
nasopharyngeal carcinoma
proliferation
metastasis
apoptosis
