Genome-wide analysis of histone modification alteration in EBV(+) GC cell lines (4C-Seq).
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ABSTRACT:
PROVIDER: PRJNA557670 | ENA |
REPOSITORIES: ENA
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Project description:Genome-wide analysis of histone modification alteration in EBV(+) GC cell lines
| PRJNA557664 | ENA
Project description:We analysed epigenetic status in EBV(+) GC cell lines to elucidate their contribution to tumorigenesis by performing ChIP-seq on H3K4me3, H3K4me1, H3K27ac, H3K27me3 and H3K9me3.
2020-05-23 | GSE135174 | GEO
Project description:Genome-wide analysis of histone modification alteration in EBV(+) GC cell lines (ChIP-Seq).
| PRJNA557671 | ENA
Project description:We analysed epigenetic status in EBV(+) GC cell lines to elucidate their contribution to tumorigenesis by performing ChIP-seq on H3K4me3, H3K4me1, H3K27ac, H3K27me3 and H3K9me3.
2020-05-23 | GSE135175 | GEO
Project description:The better prognosis of patients with Epstein-Barr virus-positive gastric carcinoma than those with EBV-negative GC is correlated with the degree of recruitment of inflammatory tumor infiltrating cells (TIL) to the vicinity of tumor cells. We hypothesized that the better prognosis would associate with less genetic or epigenetic alterations in EBV(+)GC, or EBV infection should deregulate immune modulator proteins, of which secretion recruit TIL. Therefore we performed mRNA expression profilings in EBV(-)GC and EBV(+)GC, each of which was pair wise compared with their normal control. We found that EBV(+)GC had much more molecular homogeneity with focused alterations in immune modulator genes; The Pearson correlation matrix analyses demonstrated that EBV(+)GC tumor showed remarkably high tumor homogeneity. While EBV(-)GC had considerable number genes that are differentially expressed genes from their normal counterparts, EBV(+)GC showed only a handful, almost 20 fold less number of DEG than EBV(-)GC under the same p value cutoff (p<0.001). Gene ontology and pathway analyses showed that while pathways of cation homeostasis, digestion and ion transport were commonly deregulated in both GC types, genes for chromatin assembly, prostaglandin receptor activity, pattern specification process are selectively deregulated in EBV(-)GC tumors. In contrast, pathways or genes for cytokine activity, immune response and lipoprotein particle clearance are selectively deregulated in EBV(+)GC tumors. These results demonstrate that EBV(+)GC inherently evolves to high homogeneity with fewer changes in gene expression and these secret immune modulatory chemokines could recruit reactive immune cells to EBV(+)GC, leading to favorable microenvironment for cancer suppression. All patients underwent the surgery for advanced gastric carcinoma (GC) except one patient with early GC. The EBV-presence in the GC was verified by in situ EBV-encoded small RNA (ERER) staining.. The 14 paired EBV(-)GC patients and 12 paired EBV(+)GC patients were selected for this study. Tumor tissue (T)and normal tissues (N) from distant sites from tumor areas were dissected, frozen at -80C and were subjected to RNA purification, mRNA array profiling analyses.
2014-03-01 | E-GEOD-51575 | biostudies-arrayexpress
Project description:The better prognosis of patients with Epstein-Barr virus-positive gastric carcinoma than those with EBV-negative GC is correlated with the degree of recruitment of inflammatory tumor infiltrating cells (TIL) to the vicinity of tumor cells. We hypothesized that the better prognosis would associate with less genetic or epigenetic alterations in EBV(+)GC, or EBV infection should deregulate immune modulator proteins, of which secretion recruit TIL. Therefore we performed mRNA expression profilings in EBV(-)GC and EBV(+)GC, each of which was pair wise compared with their normal control. We found that EBV(+)GC had much more molecular homogeneity with focused alterations in immune modulator genes; The Pearson correlation matrix analyses demonstrated that EBV(+)GC tumor showed remarkably high tumor homogeneity. While EBV(-)GC had considerable number genes that are differentially expressed genes from their normal counterparts, EBV(+)GC showed only a handful, almost 20 fold less number of DEG than EBV(-)GC under the same p value cutoff (p<0.001). Gene ontology and pathway analyses showed that while pathways of cation homeostasis, digestion and ion transport were commonly deregulated in both GC types, genes for chromatin assembly, prostaglandin receptor activity, pattern specification process are selectively deregulated in EBV(-)GC tumors. In contrast, pathways or genes for cytokine activity, immune response and lipoprotein particle clearance are selectively deregulated in EBV(+)GC tumors. These results demonstrate that EBV(+)GC inherently evolves to high homogeneity with fewer changes in gene expression and these secret immune modulatory chemokines could recruit reactive immune cells to EBV(+)GC, leading to favorable microenvironment for cancer suppression.
2014-03-01 | GSE51575 | GEO
Project description:We analysed gene expression in EBV(+) GC cell lines to elucidate their contribution to tumorigenesis by performing RNA-seq. Besides, we performed RNA-seq in normal gastric epithelial cells before and after EBV infection to elucidate expression changes after EBV infection.
2020-05-23 | GSE147152 | GEO
Project description: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.
2017-08-21 | GSE97837 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2020-05-23 | GSE135176 | GEO
Project description:We analysed epigenetic alterations by EBV infection especially at enhancer regions, to elucidate their contribution to tumorigenesis. We performed ChIP-seq on H3K4me3, H3K4me1, H3K27ac, H3K27me3 and H3K9me3 using gastric epithelial cells with or without EBV infection. We showed that repressive marks were redistributed after EBV infection, resulting in aberrant enhancer activation and repression. Enhancer dysfunction leads to activation of pathway related to cancer hallmarks (e.g. resisting cell death, disrupting cellular energetics, activation invasion, evading growth suppressors, sustaining proliferative signaling, angiogenesis and tumor promoting inflammation) and inactivation of tumour suppressive pathway. Dysregulation of cancer-related genes during in vitro EBV infection were also observed in EBV+ gastric cancer patients. Our analysis showed that EBV-infection associated epigenetic alteration may contribute to tumorigenesis through enhancer activation and repression.
2017-08-21 | GSE97838 | GEO