Evidence map›Paper›PMID 28801683›Full record

ArticleScientific reports2017

Regulation of tumour related genes by dynamic epigenetic alteration at enhancer regions in gastric epithelial cells infected by Epstein-Barr virus.

Atsushi Okabe, Sayaka Funata, Keisuke Matsusaka, Hiroe Namba, Masaki Fukuyo, Bahityar Rahmutulla, Motohiko Oshima, Atsushi Iwama, Masashi Fukayama, Atsushi Kaneda

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.3field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 48 citations in OpenAlex.

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  12. DNMT1 Gene Expression in Patients withTheScientificWorldJournal · 2022
    Article
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  14. Oncogenic Viruses as Entropic Drivers of Cancer Evolution.Frontiers in virology (Lausanne, Switzerland) · 2021
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Atsushi OkabeDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Sayaka FunataDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Keisuke MatsusakaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Hiroe NambaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Masaki FukuyoDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Bahityar RahmutullaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Motohiko OshimaDepartment of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Atsushi IwamaDepartment of Cellular and Molecular Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Masashi FukayamaDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Atsushi KanedaDepartment of Molecular Oncology, Graduate School of Medicine, Chiba University, Chiba, Japan. kaneda@chiba-u.jp.ORCID 0000-0002-6980-5515
Chiba University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epstein-Barr virus (EBV) infection is associated with tumours such as Burkitt lymphoma, nasopharyngeal carcinoma, and gastric cancer. We previously showed that EBV(+) gastric cancer presents an extremely high-methylation epigenotype and this aberrant DNA methylation causes silencing of multiple tumour suppressor genes. However, the mechanisms that drive EBV infection-mediated tumorigenesis, including other epigenomic alteration, remain unclear. We analysed epigenetic alterations induced by EBV infection especially at enhancer regions, to elucidate their contribution to tumorigenesis. We performed ChIP sequencing on H3K4me3, H3K4me1, H3K27ac, H3K27me3, and H3K9me3 in gastric epithelial cells infected or not with EBV. We showed that repressive marks were redistributed after EBV infection, resulting in aberrant enhancer activation and repression. Enhancer dysfunction led to the activation of pathways related to cancer hallmarks (e.g., resisting cell death, disrupting cellular energetics, inducing invasion, evading growth suppressors, sustaining proliferative signalling, angiogenesis, and tumour-promoting inflammation) and inactivation of tumour suppressive pathways. Deregulation of cancer-related genes in EBV-infected gastric epithelial cells was also observed in clinical EBV(+) gastric cancer specimens. Our analysis showed that epigenetic alteration associated with EBV-infection may contribute to tumorigenesis through enhancer activation and repression.

Indexed as

Cell Transformation, ViralEnhancer Elements, GeneticEpigenesis, GeneticCell Line, TumorChromatin ImmunoprecipitationDNA MethylationEpithelial CellsHerpesvirus 4, HumanHistonesHumansModels, BiologicalProtein BindingSequence Analysis, DNAStomach NeoplasmsHistones

Identifiers

PMID28801683
PMCPMC5554293
OpenAlexW2743865413

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.