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Histone modification alteration coordinated with acquisition of promoter DNA methylation during Epstein-Barr virus infection
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- Shogo Yamamoto
- Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan
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- Sayaka Funata
- Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan
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- Keisuke Matsusaka
- Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan
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- Ryota Yamanaka
- Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan
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- Hiroyuki Aburatani
- Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan
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- Atsushi Okabe
- Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan
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- Atsushi Kaneda
- Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan
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- Masaki Fukuyo
- Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan
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- Masashi Fukayama
- Department of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
Bibliographic Information
- Published
- 2017-07-21
- Resource Type
- journal article
- DOI
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- 10.18632/oncotarget.19423
- Publisher
- Impact Journals, LLC
Description
Aberrant DNA hypermethylation is a major epigenetic mechanism to inactivate tumor suppressor genes in cancer. Epstein-Barr virus positive gastric cancer is the most frequently hypermethylated tumor among human malignancies. Herein, we performed comprehensive analysis of epigenomic alteration during EBV infection, by Infinium HumanMethylation 450K BeadChip for DNA methylation and ChIP-sequencing for histone modification alteration during EBV infection into gastric cancer cell line MKN7. Among 7,775 genes with increased DNA methylation in promoter regions, roughly half were "DNA methylation-sensitive" genes, which acquired DNA methylation in the whole promoter regions and thus were repressed. These included anti-oncogenic genes, e.g.
Journal
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- Oncotarget
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Oncotarget 8 (33), 55265-55279, 2017-07-21
Impact Journals, LLC
