中文摘要：

目的分析甲基丙烯酸环氧丙酯（glycidyl methacrylate,GMA）致人支气管上皮细胞（16HBE细胞）恶性转化过程中不同时点全基因组甲基化水平的改变,探讨GMA诱导16HBE细胞全基因组甲基化水平改变的意义。方法通过细胞毒性试验,确定8μg/ml浓度GMA诱导16HBE细胞,收集GMA转化前期（第10代）、转化中期（第20代）、转化后期（第30代）细胞和同步溶剂对照（DMSO）细胞,以及去甲基化制剂（5-氮杂-2-脱氧胞苷,5-aza-cdr）处理的各时点转化细胞,应用DNA甲基化定量检测试剂盒,检测不同转化时期细胞全基因组甲基化水平。结果 DNA甲基化定量检测结果显示,不同时点GMA转化组较同代龄DMSO组细胞全基因组甲基化水平降低,转化前期GMA组、DMSO组、5-aza-cdr组细胞甲基化水平较转化中期及转化后期相对应各组的全基因组甲基化水平低。结论 GMA诱导16HBE细胞在转化前期已出现全基因组低甲基化现象,故可将其视为细胞恶性转化前期生物标志。

英文摘要：

Objective To analyze the changes of the whole-genome methylation level at different stages of malignant transformation of human bronchial epithelial cells （16HBE） induced by glyeidylmethacrylate （GMA） and discussing the effect of whole-genome methylation level change in the process. Methods By cytotoxicity test, determining GMA （8 μg/ml） transformed 16HBE cell. Harvesting and extracting DNA from transformed cells, DMSO control group cell, 5-aza-cdr group cell at protophase （the 10th generation）, metaphase （the 20th generation） and anaphase （the 30th generation）. Adopting MethyflashTM Methylated DNA Quantification Kit （Colorimetrie） to detect the genome-wide methylation levels at different transformed stages. Results DNA methylation quantitative test results showed that the methylation levels GMA group was lower than that in the same generation of DMSO group at different transformed stages, and protophase （DMSO group, GMA group, 5-aza-cdr group） was lower than that in metaphase and anaphase in corresponding group. Conclusion The phenomenon of whole-genome low methylation induced by GMA transformed 16HBE cells has occurred in protophase, which can be used as an early biomarker of malignant transformation.