Evidence map›Paper›PMID 36574362›Full record

ArticleThe EMBO journal2023

DNA damage repair kinase DNA-PK and cGAS synergize to induce cancer-related inflammation in glioblastoma.

Clara Taffoni, Johanna Marines, Hanane Chamma, Soumyabrata Guha, Mathilde Saccas, Amel Bouzid, Ana-Luiza Chaves Valadao, Clément Maghe, Jane Jardine, Mi Kyung Park and 15 more

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 31 citations in OpenAlex.

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  9. Mitochondrial DNA as a driver of inflammation via the cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

25 authors at 4 institutions in 2 countries.

Clara Taffoni *IGH, Université de Montpellier, CNRS, Montpellier, France.ORCID 0000-0001-9265-5909
Johanna Marines *IGH, Université de Montpellier, CNRS, Montpellier, France.
Hanane ChammaIGH, Université de Montpellier, CNRS, Montpellier, France.
Soumyabrata GuhaIGH, Université de Montpellier, CNRS, Montpellier, France.ORCID 0000-0002-8996-6340
Mathilde SaccasIGH, Université de Montpellier, CNRS, Montpellier, France.
Amel BouzidIGH, Université de Montpellier, CNRS, Montpellier, France.
Ana-Luiza Chaves ValadaoIGH, Université de Montpellier, CNRS, Montpellier, France.
Clément MagheTeam SOAP, CRCI2NA, Nantes Université, Inserm, CNRS, Université d'Angers, Nantes, France.
Jane JardineTeam SOAP, CRCI2NA, Nantes Université, Inserm, CNRS, Université d'Angers, Nantes, France.
Mi Kyung ParkDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID 0000-0003-1273-4311
Katarzyna PolakIGH, Université de Montpellier, CNRS, Montpellier, France.
Mara De MartinoDepartment of Radiation Oncology, Weill Cornell Medicine, New York, NY, USA.ORCID 0000-0002-3049-6495
Claire Vanpouille-BoxDepartment of Radiation Oncology, Weill Cornell Medicine, New York, NY, USA.ORCID 0000-0001-7213-0670
Maguy Del RioInstitut de Recherche en Cancérologie de Montpellier (IRCM), INSERM, Université de Montpellier, ICM, Montpellier, France.
Celine GongoraInstitut de Recherche en Cancérologie de Montpellier (IRCM), INSERM, Université de Montpellier, ICM, Montpellier, France.
Julie GavardTeam SOAP, CRCI2NA, Nantes Université, Inserm, CNRS, Université d'Angers, Nantes, France.ORCID 0000-0002-7985-9007
Nicolas BidèreTeam SOAP, CRCI2NA, Nantes Université, Inserm, CNRS, Université d'Angers, Nantes, France.ORCID 0000-0001-9177-0008
Min Sup SongDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Donovan PineauInstitut de Génomique Fonctionnelle (IGF), Université de Montpellier, CNRS, INSERM, Montpellier, France.
Jean-Philippe HugnotInstitut de Génomique Fonctionnelle (IGF), Université de Montpellier, CNRS, INSERM, Montpellier, France.
Karima KissaUniversité de Montpellier, CNRS UMR 5235, Montpellier, France.
Laura FontenilleAzelead©, Montpellier, France.
Fabien P BlanchetInstitut de Recherche en Infectiologie de Montpellier, Université de Montpellier, CNRS, Montpellier, France.ORCID 0000-0003-3168-0697
Isabelle K VilaIGH, Université de Montpellier, CNRS, Montpellier, France.
Nadine LaguetteIGH, Université de Montpellier, CNRS, Montpellier, France.ORCID 0000-0001-8072-5607
Centre National de la Recherche Scientifique · FRCornell University · USInserm · FRThe University of Texas MD Anderson Cancer Center · US

Funding

The role of PTEN feedback mechanism in cancerR01CA196740 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Min Sup Song · 2016 to 2026
$3.4M
Targeting m6A RNA epigenetics in treatment-emergent neuroendocrine prostate cancerR01CA258100 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SONG, MIN SUP · 2021 to 2025
$1.8M
European Research Council 637763NCI NIH HHS R01 CA196740NCI NIH HHS R01 CA258100
6 · The paper itself

Abstract

Cytosolic DNA promotes inflammatory responses upon detection by the cyclic GMP-AMP (cGAMP) synthase (cGAS). It has been suggested that cGAS downregulation is an immune escape strategy harnessed by tumor cells. Here, we used glioblastoma cells that show undetectable cGAS levels to address if alternative DNA detection pathways can promote pro-inflammatory signaling. We show that the DNA-PK DNA repair complex (i) drives cGAS-independent IRF3-mediated type I Interferon responses and (ii) that its catalytic activity is required for cGAS-dependent cGAMP production and optimal downstream signaling. We further show that the cooperation between DNA-PK and cGAS favors the expression of chemokines that promote macrophage recruitment in the tumor microenvironment in a glioblastoma model, a process that impairs early tumorigenesis but correlates with poor outcome in glioblastoma patients. Thus, our study supports that cGAS-dependent signaling is acquired during tumorigenesis and that cGAS and DNA-PK activities should be analyzed concertedly to predict the impact of strategies aiming to boost tumor immunogenicity.

Indexed as

DNA-Activated Protein KinaseGlioblastomaNucleotidyltransferasesCarcinogenesisCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNADNA DamageDNA RepairHumansImmunity, InnateInflammationTumor MicroenvironmentcGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNADNA-Activated Protein KinaseNucleotidyltransferasesPRKDC protein, humancGASDNA-PKinflammationtumor immunogenicity

Identifiers

PMID36574362
PMCPMC10068334
OpenAlexW4312210106

What OpenQuestion holds

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LicenceCC BY
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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.