Evidence map›Paper›PMID 22721696›Full record

ArticleExperimental cell research2012

Downregulation of SWI/SNF chromatin remodeling factor subunits modulates cisplatin cytotoxicity.

Anbarasi Kothandapani, Kathirvel Gopalakrishnan, Bhaskar Kahali, David Reisman, Steve M Patrick

Abstract read
In one paragraph

Article in Experimental cell research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

47 citing papers in PubMed, 65 citations in OpenAlex.

  1. BRM Promoter Polymorphisms and Survival of Advanced Non-Small Cell Lung Cancer Patients in the Princess Margaret Cohort and CCTG BR.24 Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Trial
  2. Article
  3. Article
  4. The role of SMARCA4 in lung cancer.Scientific reports · 2025
    Review
  5. Review
  6. Review
  7. Translational lung cancer research · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. ARID1A Mutation May Define an Immunologically Active Subgroup in Patients with Microsatellite Stable Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  19. Article
  20. ACTL6A promotes repair of cisplatin-induced DNA damage, a new mechanism of platinum resistance in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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

5 authors at 2 institutions in 1 country.

Anbarasi KothandapaniDepartment of Biochemistry and Cancer Biology, University of Toledo-Health Science Campus, Toledo, OH 43614, USA.
Kathirvel Gopalakrishnan
Bhaskar Kahali
David Reisman
Steve M Patrick
University of Florida · USUniversity of Toledo · US

Funding

UF Clinical and Translational Science AwardUL1TR000064 · NCATS · UNIVERSITY OF FLORIDA · PI NELSON, DAVID R · 2012 to 2014
$12.2M
Novel Role of Base Excision Repair and Mismatch Repair in Cisplatin SensitivityR01GM088249 · NIGMS · WAYNE STATE UNIVERSITY · PI PATRICK, STEVE M · 2010 to 2014
$1.4M
NCATS NIH HHS UL1 TR000064NIGMS NIH HHS GM088249NIGMS NIH HHS R01 GM088249
6 · The paper itself

Abstract

Chromatin remodeling complex SWI/SNF plays important roles in many cellular processes including transcription, proliferation, differentiation and DNA repair. In this report, we investigated the role of SWI/SNF catalytic subunits Brg1 and Brm in the cellular response to cisplatin in lung cancer and head/neck cancer cells. Stable knockdown of Brg1 and Brm enhanced cellular sensitivity to cisplatin. Repair kinetics of cisplatin DNA adducts revealed that downregulation of Brg1 and Brm impeded the repair of both intrastrand adducts and interstrand crosslinks (ICLs). Cisplatin ICL-induced DNA double strand break repair was also decreased in Brg1 and Brm depleted cells. Altered checkpoint activation with enhanced apoptosis as well as impaired chromatin relaxation was observed in Brg1 and Brm deficient cells. Downregulation of Brg1 and Brm did not affect the recruitment of DNA damage recognition factor XPC to cisplatin DNA lesions, but affected ERCC1 recruitment, which is involved in the later stages of DNA repair. Based on these results, we propose that SWI/SNF chromatin remodeling complex modulates cisplatin cytotoxicity by facilitating efficient repair of the cisplatin DNA lesions.

Indexed as

Antineoplastic AgentsCarcinoma, Non-Small-Cell LungCell Line, TumorChromatinChromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneCisplatinDNA AdductsDNA-Binding ProteinsDNA HelicasesDNA RepairEndonucleasesGene Expression Regulation, NeoplasticGene Knockdown TechniquesHead and Neck NeoplasmsHumansAntineoplastic AgentsChromatinChromosomal Proteins, Non-HistoneCisplatincisplatin-DNA adductDNA AdductsDNA-Binding ProteinsDNA HelicasesEndonucleasesERCC1 protein, humanNuclear ProteinsProtein SubunitsRNA, Small InterferingSMARCA2 protein, humanSMARCA4 protein, humanSWI-SNF-B chromatin-remodeling complexTranscription FactorsXPC protein, human

Identifiers

PMID22721696
PMCPMC3408789
OpenAlexW2050540286

What OpenQuestion holds

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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.