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Series GSE97837 Query DataSets for GSE97837
Status Public on Aug 21, 2017
Title Histone modification (H3K4me3, H3K27ac, and H3K27me3) change during EBV infection in gastric epithelial cells
Organism Homo sapiens
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary Aberrant DNA hypermethylation is a major epigenetic mechanism to inactivate tumor suppressor genes in cancer, and Epstein-Barr virus (EBV) positive gastric cancer is known as the most frequently hypermethylated tumor among whole human malignancies. We here performed comprehensive analysis of epigenomic alteration during EBV infection, by Infinium HumanMethylation 450K BeadChip for DNA methylation and ChIP-sequencing for histone modification alteration. While 7,727 genes showed increase of DNA methylation in a promoter region, roughly half of these were “DNA methylation-sensitive” genes including anti-oncogenic genes e.g. CDKN2A and CDH1, which acquired DNA methylation in the whole promoter regions, thus leading to gene repression. Another half were “DNA methylation-resistant” genes including DNA repair genes, where DNA methylation is acquired in the surrounding of promoter regions but unmethylated status is protected in the vicinity of transcription start site, with gene expression retained. Histone modification alteration also occurred dynamically during EBV infection, in coordinated manner with DNA methylation alteration. DNA methylation-sensitive genes significantly correlated with loss of H3K27me3 pre-marks or decrease of active histone marks e.g. H3K4me3 and H3K27ac, and apoptosis-related genes were significantly enriched in these epigenetically repressed genes. Gain of active histone marks significantly correlated with DNA methylation-resistant genes, and genes related to mitotic cell cycle and DNA repair were significantly enriched in these epigenetically activated genes. Orchestrated epigenetic alterations play an important role in gene regulation during EBV infection, and histone modification status in promoter regions significantly associated with acquisition of de novo DNA methylation or protection of unmethylated status at TSS.
Overall design Examination of 3 different histone modifications in EBV infected or uninfected gastric cancer cells.
Contributor(s) Funata S, Okabe A, Fukuyo M, Kaneda A
Citation(s) 28801683, 32119176
Submission date Apr 14, 2017
Last update date May 26, 2020
Contact name Masaki Fukuyo
Organization name Chiba University
Department Department of Molecular Oncology
Street address 1-8-1 Inohana, Chuo-ku
City Chiba
ZIP/Postal code 260-8670
Country Japan
Platforms (2)
GPL10999 Illumina Genome Analyzer IIx (Homo sapiens)
GPL18460 Illumina HiSeq 1500 (Homo sapiens)
Samples (6)
GSM2579147 MKN7_wt_H3K4me3
GSM2579148 MKN7_wt_H3K27ac
GSM2579149 MKN7_wt_H3K27me3
BioProject PRJNA382993
SRA SRP103947

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Supplementary file Size Download File type/resource
GSE97837_RAW.tar 922.0 Mb (http)(custom) TAR (of BIGWIG)
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Raw data are available in SRA
Processed data provided as supplementary file

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