A genome-wide study of DNA methylation modified by epigallocatechin-3-gallate in the CAL-27 cell line

被引:15
作者
Chen, Li-Li [1 ,2 ]
Han, Wen-Fei [1 ]
Geng, Ying [1 ]
Su, Jian-Sheng [1 ]
机构
[1] Tongji Univ, Sch Stomatol, Lab Oral Biomed Sci & Translat Med, Shanghai 200072, Peoples R China
[2] Xiamen Univ, Zhongshan Hosp, Dept Stomatol, Xiamen 361004, Fujian, Peoples R China
基金
美国国家科学基金会;
关键词
epigallocatechin-3-gallate; epigenetics; cancer; methylation; GREEN TEA POLYPHENOL; CARCINOMA-CELLS; CANCER CELLS; SIGNALING PATHWAYS; EGCG; (-)-EPIGALLOCATECHIN-3-GALLATE; GALLATE; SUPPRESSION; INHIBITION; MECHANISMS;
D O I
10.3892/mmr.2015.4118
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
In order to gain greater understanding of the mechanisms underlying the effect of epigallocatechin-3-gallate (EGCG) On DNA methylation and its chemopreventative action in oral squamous cell carcinoma (OSCC), a genome-wide methylation and mRNA expression screen was performed in the CAL-27 cell line with and without EGCG (100 mu M) treatment. A total of 761 differentially methylated gene loci were identified following treatment with EGCG. Comparison of gene expression profiling in OSCC samples revealed 184 transcripts with a significant difference (P<0.05) and a fold change difference >2 compared with controls. Gene ontology analysis of differentially methylated loci and functional annotation of the differentially expressed genes indicated that the main pathways involved were metabolic, mitogen-activated protein kinase (MAPK), wilt, and cell cycle pathways. In conclusion, the present study indicates that EGCG can affect the methylation status and gene expression in the CAL-27 cell line. Additionally, the changes in several important signaling pathways may reveal the antitumor mechanism of EGCG.
引用
收藏
页码:5886 / 5890
页数:5
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