Evidence map›Paper›PMID 25071011›Full record

ArticleOncotarget2014

Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes.

Veronika Vlková, Ivan Štěpánek, Veronika Hrušková, Filip Šenigl, Veronika Mayerová, Martin Šrámek, Jana Šímová, Jana Bieblová, Marie Indrová, Tomáš Hejhal and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

26 citing papers in PubMed, 40 citations in OpenAlex.

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  17. Cell-mediated immune resistance in cancer.Cancer drug resistance (Alhambra, Calif.) · 2020
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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

14 authors at 3 institutions in 2 countries.

Veronika VlkováDepartment of Tumour Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, v. v. i., Prague.
Ivan ŠtěpánekDepartment of Tumour Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, v. v. i., Prague.
Veronika HruškováDepartment of Tumour Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, v. v. i., Prague.
Filip ŠeniglDepartment of Viral and Cellular Genetics, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, v. v. i., Prague.
Veronika MayerováDepartment of Tumour Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, v. v. i., Prague.
Martin ŠrámekDepartment of Tumour Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, v. v. i., Prague.
Jana ŠímováDepartment of Tumour Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, v. v. i., Prague.
Jana BieblováDepartment of Tumour Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, v. v. i., Prague.
Marie IndrováDepartment of Tumour Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, v. v. i., Prague.
Tomáš HejhalDepartment of Tumour Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, v. v. i., Prague.
Nicolas DérianUPMC Univ Paris 06, UMR 7211, Immunology-Immunopathology-Immunotherapy (I3), Paris, France; CNRS, UMR 7211, Immunology-Immunopathology-Immunotherapy (I3), Paris, France; INSERM, UMR_S 959, Immunology-Immunopathology-Immunotherapy (I3), Paris, France; AP-HP, Hôpital Pitié-Salpêtrière, CIC-BTi Biotherapy & Département Hospitalo-Universitaire (DHU) Inflammation-Immunopathology-Biotherapy (i2B), Paris, France.
David KlatzmannUPMC Univ Paris 06, UMR 7211, Immunology-Immunopathology-Immunotherapy (I3), Paris, France; CNRS, UMR 7211, Immunology-Immunopathology-Immunotherapy (I3), Paris, France; INSERM, UMR_S 959, Immunology-Immunopathology-Immunotherapy (I3), Paris, France; AP-HP, Hôpital Pitié-Salpêtrière, CIC-BTi Biotherapy & Département Hospitalo-Universitaire (DHU) Inflammation-Immunopathology-Biotherapy (i2B), Paris, France.
Adrien SixUPMC Univ Paris 06, UMR 7211, Immunology-Immunopathology-Immunotherapy (I3), Paris, France; CNRS, UMR 7211, Immunology-Immunopathology-Immunotherapy (I3), Paris, France; INSERM, UMR_S 959, Immunology-Immunopathology-Immunotherapy (I3), Paris, France; AP-HP, Hôpital Pitié-Salpêtrière, CIC-BTi Biotherapy & Département Hospitalo-Universitaire (DHU) Inflammation-Immunopathology-Biotherapy (i2B), Paris, France.
Milan ReinišDepartment of Tumour Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, v. v. i., Prague.
Czech Academy of Sciences · CZCentre National de la Recherche Scientifique · FRCzech Academy of Sciences, Institute of Molecular Genetics · CZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Downregulation of MHC class I expression on tumour cells, a common mechanism by which tumour cells can escape from specific immune responses, can be associated with coordinated silencing of antigen-presenting machinery genes. The expression of these genes can be restored by IFNγ. In this study we documented association of DNA demethylation of selected antigen-presenting machinery genes located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFNγ treatment with MHC class I upregulation on tumour cells in several MHC class I-deficient murine tumour cell lines (TC-1/A9, TRAMP-C2, MK16 and MC15). Our data also documented higher methylation levels in these genes in TC-1/A9 cells, as compared to their parental MHC class I-positive TC-1 cells. IFNγ-mediated DNA demethylation was relatively fast in comparison with demethylation induced by DNA methyltransferase inhibitor 5-azacytidine, and associated with increased histone H3 acetylation in the promoter regions of APM genes. Comparative transcriptome analysis in distinct MHC class I-deficient cell lines upon their treatment with either IFNγ or epigenetic agents revealed that a set of genes, significantly enriched for the antigen presentation pathway, was regulated in the same manner. Our data demonstrate that IFNγ acts as an epigenetic modifier when upregulating the expression of antigen-presenting machinery genes.

Indexed as

DNA MethylationGenes, MHC Class IAnimalsAntigen PresentationDown-RegulationEpigenesis, GeneticFibrosarcomaGene Expression Regulation, NeoplasticInterferon-gammaMiceMice, Inbred C57BLSignal TransductionTransfectionTumor Cells, CulturedUp-RegulationInterferon-gamma

Identifiers

PMID25071011
PMCPMC4196173
OpenAlexW2135320283

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Registered trials

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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.