Histone modification alteration coordinated with acquisition of promoter DNA methylation during Epstein-Barr virus infection

  • Sayaka Funata
    Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan
  • Keisuke Matsusaka
    Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan
  • Ryota Yamanaka
    Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan
  • Shogo Yamamoto
    Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan
  • Atsushi Okabe
    Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan
  • Masaki Fukuyo
    Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan
  • Hiroyuki Aburatani
    Genome Science Division, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan
  • Masashi Fukayama
    Department of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
  • Atsushi Kaneda
    Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan

説明

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.

収録刊行物

  • Oncotarget

    Oncotarget 8 (33), 55265-55279, 2017-07-21

    Impact Journals, LLC

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