Evidence map›Paper›PMID 30287812›Full record

ArticleNature communications2018

DNA damage sensitivity of SWI/SNF-deficient cells depends on TFIIH subunit p62/GTF2H1.

Cristina Ribeiro-Silva, Özge Z Aydin, Raquel Mesquita-Ribeiro, Jana Slyskova, Angela Helfricht, Jurgen A Marteijn, Jan H J Hoeijmakers, Hannes Lans, Wim Vermeulen

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-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

22 citing papers in PubMed, 37 citations in OpenAlex.

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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

9 authors at 3 institutions in 3 countries.

Cristina Ribeiro-SilvaDepartment of Molecular Genetics, Oncode Institute, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands.ORCID http://orcid.org/0000-0002-2102-1949
Özge Z AydinDepartment of Molecular Genetics, Oncode Institute, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands.
Raquel Mesquita-RibeiroSchool of Life Sciences, University of Nottingham, NG7 2UH, Nottingham, United Kingdom.
Jana SlyskovaDepartment of Molecular Genetics, Oncode Institute, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands.
Angela HelfrichtDepartment of Molecular Genetics, Oncode Institute, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands.
Jurgen A MarteijnDepartment of Molecular Genetics, Oncode Institute, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands.
Jan H J HoeijmakersDepartment of Molecular Genetics, Oncode Institute, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands.
Hannes LansDepartment of Molecular Genetics, Oncode Institute, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands. w.lans@erasmusmc.nl.ORCID http://orcid.org/0000-0003-4417-5358
Wim VermeulenDepartment of Molecular Genetics, Oncode Institute, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, The Netherlands. w.vermeulen@erasmusmc.nl.
Erasmus MC · NLKoç University · TRUniversity of Nottingham · GB

Funding

EC | European Research Council (ERC) 340988European Commission (EC) 316390European Research Council 340988KWF Kankerbestrijding (Dutch Cancer Society) 10506Nederlandse Organisatie voor Wetenschappelijk Onderzoek (Netherlands Organisation for Scientific Research) 854.11.002 and 864.13.004Worldwide Cancer Research 15-1274
6 · The paper itself

Abstract

Mutations in SWI/SNF genes are amongst the most common across all human cancers, but efficient therapeutic approaches that exploit vulnerabilities caused by SWI/SNF mutations are currently lacking. Here, we show that the SWI/SNF ATPases BRM/SMARCA2 and BRG1/SMARCA4 promote the expression of p62/GTF2H1, a core subunit of the transcription factor IIH (TFIIH) complex. Inactivation of either ATPase subunit downregulates GTF2H1 and therefore compromises TFIIH stability and function in transcription and nucleotide excision repair (NER). We also demonstrate that cells with permanent BRM or BRG1 depletion have the ability to restore GTF2H1 expression. As a consequence, the sensitivity of SWI/SNF-deficient cells to DNA damage induced by UV irradiation and cisplatin treatment depends on GTF2H1 levels. Together, our results expose GTF2H1 as a potential novel predictive marker of platinum drug sensitivity in SWI/SNF-deficient cancer cells.

Indexed as

DNA RepairCell LineDNA DamageDNA HelicasesHumansNuclear ProteinsPhosphoproteinsTranscription FactorsTranscription Factors, TFIITranscription Factor TFIIHDNA HelicasesGTF2H1 protein, humanNuclear ProteinsPhosphoproteinsSMARCA2 protein, humanSMARCA4 protein, humanTranscription FactorsTranscription Factors, TFIITranscription Factor TFIIH

Identifiers

PMID30287812
PMCPMC6172278
OpenAlexW2892858628

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.