Evidence map›Paper›PMID 33742126›Full record

ArticleOncogene2021

ARID2 deficiency promotes tumor progression and is associated with higher sensitivity to chemotherapy in lung cancer.

Thaidy Moreno, Beatriz Monterde, Laura González-Silva, Isabel Betancor-Fernández, Carlos Revilla, Antonio Agraz-Doblas, Javier Freire, Pablo Isidro, Laura Quevedo, Rosa Blanco and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2021. 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
2.6field-weighted citation impact, top 9% 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, 39 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Single-Cell Transcriptomic Landscape Deciphers Intratumoral Heterogeneity and Subtypes of Acral and Mucosal Melanomas.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Article
  6. Current issues in molecular biology · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Aging-Associated ALKBH5-mJournal of the American Heart Association · 2024
    Article
  12. Review
  13. (mis)-Targeting of SWI/SNF complex(es) in cancer.Cancer metastasis reviews · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

20 authors at 4 institutions in 2 countries.

Thaidy MorenoInstituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC, Santander, Spain.
Beatriz MonterdeInstituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC, Santander, Spain.
Laura González-SilvaInstituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC, Santander, Spain.ORCID http://orcid.org/0000-0001-8625-1473
Isabel Betancor-FernándezDepartamento de Patología, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Tenerife, Spain.
Carlos RevillaInstituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC, Santander, Spain.
Antonio Agraz-DoblasInstituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC, Santander, Spain.
Javier FreireServicio de Anatomía Patológica y Biobanco Valdecilla, HUMV/IDIVAL, Santander, Spain.
Pablo IsidroBiobanco del Principado de Asturias (BBPA), Hospital Universitario Central de Asturias, Oviedo, Spain.
Laura QuevedoInstituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC, Santander, Spain.ORCID http://orcid.org/0000-0001-8902-5818
Rosa BlancoInstituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC, Santander, Spain.
Santiago Montes-MorenoServicio de Anatomía Patológica y Biobanco Valdecilla, HUMV/IDIVAL, Santander, Spain.
Laura CerecedaServicio de Anatomía Patológica y Biobanco Valdecilla, HUMV/IDIVAL, Santander, Spain.
Aurora AstudilloBiobanco del Principado de Asturias (BBPA), Hospital Universitario Central de Asturias, Oviedo, Spain.ORCID http://orcid.org/0000-0001-8947-8809
Berta CasarInstituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC, Santander, Spain.
Piero CrespoInstituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC, Santander, Spain.
Cristina Morales TorresCancer Epigenetics Laboratory, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0002-7126-6565
Paola ScaffidiCancer Epigenetics Laboratory, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0002-3642-4193
Javier Gómez-RománServicio de Anatomía Patológica y Biobanco Valdecilla, HUMV/IDIVAL, Santander, Spain.
Eduardo SalidoDepartamento de Patología, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Tenerife, Spain.
Ignacio VarelaInstituto de Biomedicina y Biotecnología de Cantabria, Universidad de Cantabria-CSIC, Santander, Spain. ignacio.varela@unican.es.ORCID http://orcid.org/0000-0002-0969-506X
Universidad de Cantabria · ESMarqués de Valdecilla University Hospital · ESCentre for Biomedical Network Research on Rare Diseases · ESThe Francis Crick Institute · GB

Funding

European Research Council 637904Medical Research Council FC001152Wellcome Trust FC001152
6 · The paper itself

Abstract

The survival rate in lung cancer remains stubbornly low and there is an urgent need for the identification of new therapeutic targets. In the last decade, several members of the SWI/SNF chromatin remodeling complexes have been described altered in different tumor types. Nevertheless, the precise mechanisms of their impact on cancer progression, as well as the application of this knowledge to cancer patient management are largely unknown. In this study, we performed targeted sequencing of a cohort of lung cancer patients on genes involved in chromatin structure. In addition, we studied at the protein level the expression of these genes in cancer samples and performed functional experiments to identify the molecular mechanisms linking alterations of chromatin remodeling genes and tumor development. Remarkably, we found that 20% of lung cancer patients show ARID2 protein loss, partially explained by the presence of ARID2 mutations. In addition, we showed that ARID2 deficiency provokes profound chromatin structural changes altering cell transcriptional programs, which bolsters the proliferative and metastatic potential of the cells both in vitro and in vivo. Moreover, we demonstrated that ARID2 deficiency impairs DNA repair, enhancing the sensitivity of the cells to DNA-damaging agents. Our findings support that ARID2 is a bona fide tumor suppressor gene in lung cancer that may be exploited therapeutically.

Indexed as

A549 CellsAnimalsCell Line, TumorDisease ProgressionFemaleHigh-Throughput Nucleotide SequencingHumansLung NeoplasmsMiceMice, NudeSurvival RateTranscription FactorsARID2 protein, humanArid2 protein, mouseTranscription Factors

Identifiers

PMID33742126
PMCPMC7610680
OpenAlexW3136760473

What OpenQuestion holds

Textmetadata
LicenceTDM
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.