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Epstein-Barr 病毒诱导的 DNA 高甲基化在 Epstein-Barr 病毒相关性胃癌发生发展中的作用。

DNA hypermethylation induced by Epstein-Barr virus in the development of Epstein-Barr virus-associated gastric carcinoma.

机构信息

College of Pharmacy and Cancer Research Institute and Research Institute of Pharmaceutical Sciences, Kyungpook National University, Taegu, Republic of Korea.

Department of Medicinal Crop Research, National Institute of Horticultural and Herbal Science, Rural Development Administration, Eumseong, Republic of Korea.

出版信息

Arch Pharm Res. 2017 Aug;40(8):894-905. doi: 10.1007/s12272-017-0939-5. Epub 2017 Aug 4.

DOI:10.1007/s12272-017-0939-5
PMID:28779374
Abstract

Epstein-Barr virus (EBV)-associated gastric carcinoma (EBVaGC) is a recently recognized disease entity defined by the presence of EBV in gastric carcinoma cells. EBV infection causes major epigenetic alterations in the EBV genome and its cellular host genome, suggesting that EBV acts as a direct epigenetic driver for EBVaGC. One of the major epigenetic events in the viral and cellular genomes to control transcription is DNA hypo- or hyper-methylation. Particularly, local and global hypermethylation have been reported in EBVaGC. It is therefore important to understand the molecular mechanisms of DNA hypermethylation during EBVaGC carcinogenesis. To understand the functional roles of DNA methylation and suggest therapeutic target candidates for EBVaGC, we reviewed recent literature reporting DNA hypermethylation in EBVaGC. We summarized the identified candidate genes that are markedly hypermethylated in EBVaGC, which can potentially be targets for chemotherapies with demethylating agents.

摘要

EB 病毒(EBV)相关胃癌(EBVaGC)是一种最近被确认的疾病实体,其定义为胃癌细胞中存在 EBV。EBV 感染导致 EBV 基因组及其细胞宿主基因组的主要表观遗传改变,表明 EBV 是 EBVaGC 的直接表观遗传驱动因素。控制转录的病毒和细胞基因组中的主要表观遗传事件之一是 DNA 低甲基化或高甲基化。特别是,在 EBVaGC 中已经报道了局部和全局高甲基化。因此,了解 EBVaGC 癌变过程中 DNA 高甲基化的分子机制非常重要。为了了解 DNA 甲基化的功能作用,并为 EBVaGC 提出治疗靶点候选物,我们回顾了最近报道 EBVaGC 中 DNA 高甲基化的文献。我们总结了在 EBVaGC 中明显高甲基化的鉴定候选基因,这些基因可能是具有去甲基化剂的化疗药物的潜在靶点。

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