实验性舌癌发生过程中 DNA 甲基化变化的全球分析。

Hua Liu, Wanyuan Yue, Shuai Shao, Jiaping Sun, Ying Yang, Xiaoming Dai
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引用次数: 0

摘要

研究目的本研究旨在通过全面分析实验性舌癌发生过程中的全局 DNA 甲基化改变,评估 DNA 甲基化改变在舌癌中的作用:方法:给 C57BL/6J 小鼠口服 4-硝基喹啉-1-氧化物(4NQO,50 mg/L)16 周。采集代表正常组织(第 0 周)、早期(第 12 周)和晚期(第 28 周)肿瘤发生的舌粘膜样本,进行芯片和甲基化 DNA 免疫沉淀测序(MeDIP-Seq)。用实时定量反转录聚合酶链反应和 Massarray 评估了人舌粘膜和舌癌细胞系中转化生长因子-β-信号蛋白 1(SMAD1)的 mRNA 和启动子甲基化情况:结果:28周时观察到的胞嘧啶鸟嘌呤岛(CGI)甲基化水平超过了12周和0周时的水平。12 周时的启动子甲基化水平超过了 0 周时的水平。值得注意的是,208 个差异表达基因与 0、12 和 28 周启动子甲基化水平的差异呈负相关。与正常粘膜相比,细胞系中 SMAD1 的 mRNA 上调,同时启动子甲基化水平下降:结论:DNA甲基化在舌癌发生过程中发生了变化。结论:DNA甲基化在舌癌发生过程中发生了变化,SMAD1的过表达与舌癌细胞系启动子甲基化水平降低有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Global analysis of DNA methylation changes during experimented lingual carcinogenesis.

Objectives: This study aims to assess the role of DNA methylation changes in tongue cancer through a comprehensive analysis of global DNA methylation alterations during experimental lingual carcinogenesis.

Methods: C57BL/6J mice were subjected to 16-week oral administration of 4-nitroquinoline-1-oxide (4NQO, 50 mg/L). Lingual mucosa samples, being representative of normal tissue (week 0) and early (week 12) and advanced (week 28) tumorigenesis, were harvested for microarray and methylated DNA immunoprecipitation sequencing (MeDIP-Seq). The mRNA and promoter methylation of transforming growth factor-beta-signaling protein 1 (SMAD1) were evaluated with real-time quantitative reverse transcription polymerase chain reaction and Massarray in human lingual mucosa and tongue cancer cell lines.

Results: The cytosine guanine island (CGI) methylation level observed at 28 weeks surpassed that of both 12 weeks and 0 weeks. The promoter methylation level at 12 weeks exceeded that at 0 weeks. Notably, 208 differentially expressed genes were negatively correlated to differential methylation in promoters among 0, 12, and 28 weeks. The mRNA of SMAD1 was upregulated, concurrent with a decrease in promoter methylation levels in cell lines compared to normal mucosa.

Conclusions: DNA methylation changed during lingual carcinogenesis. Overexpression of SMAD1 was correlated to promoter hypomethylation in tongue cancer cell lines.

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