Evidence map›Paper›PMID 21900401›Full record

ArticleCancer research2011

ARID1A, a factor that promotes formation of SWI/SNF-mediated chromatin remodeling, is a tumor suppressor in gynecologic cancers.

Bin Guan, Tian-Li Wang, Ie-Ming Shih

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 286 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
286citing papers in PubMed, 1 pooled it
12.9field-weighted citation impact, top 1% 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

286 citing papers in PubMed, 1 synthesis or guideline pooled it, 449 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. RNA-Seq Profiling Reveals Transcriptional Changes in Phosphorylation-Site Mutants of Brg1.Genes to cells : devoted to molecular & cellular mechanisms · 2026
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226 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Bin GuanDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Tian-Li Wang
Ie-Ming Shih
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Molecular Diagnostics for Malignant EffusionR01CA103937 · NCI · JOHNS HOPKINS UNIVERSITY · PI SHIH, IE-MING · 2004 to 2012
$2.7M
The Roles of HBXAP Gene in Ovarian CancerR01CA129080 · NCI · JOHNS HOPKINS UNIVERSITY · PI SHIH, IE-MING · 2008 to 2012
$1.7M
NCI NIH HHS CA103937NCI NIH HHS CA129080NCI NIH HHS R01 CA103937NCI NIH HHS R01 CA129080
6 · The paper itself

Abstract

ARID1A (BAF250A) promotes the formation of SWI/SNF chromatin remodeling complexes containing BRG1 or BRM. It has emerged as a candidate tumor suppressor based on its frequent mutations in ovarian clear cell and endometrioid cancers and in uterine endometrioid carcinomas. Here, we report that restoring wild-type ARID1A expression in ovarian cancer cells that harbor ARID1A mutations is sufficient to suppress cell proliferation and tumor growth in mice, whereas RNA interference-mediated silencing of ARID1A in nontransformed epithelial cells is sufficient to enhance cellular proliferation and tumorigenicity. Gene expression analysis identified several downstream targets of ARID1A including CDKN1A and SMAD3, which are well-known p53 target genes. In support of the likelihood that p53 mediates the effects of ARID1A on these genes, we showed that p53 was required and sufficient for their regulation by ARID1A. Furthermore, we showed that CDKN1A (encoding p21) acted in part to mediate growth suppression by ARID1A. Finally, we obtained evidence that the ARID1A/BRG1 complex interacted directly with p53 and that mutations in the ARID1A and TP53 genes were mutually exclusive in tumor specimens examined. Our results provide functional evidence in support of the hypothesis that ARID1A is a bona fide tumor suppressor that collaborates with p53 to regulate CDKN1A and SMAD3 transcription and tumor growth in gynecologic cancers.

Indexed as

Adenocarcinoma, Clear CellAnimalsCell Line, TumorChromatin Assembly and DisassemblyCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsDNA HelicasesEpithelial CellsFemaleGene Expression Regulation, NeoplasticGenetic Complementation TestHumansMiceMice, NudeMultiprotein ComplexesMutationARID1A protein, humanCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DNA-Binding ProteinsDNA HelicasesMultiprotein ComplexesNeoplasm ProteinsNuclear Proteinsp21-Activated KinasesPak1 protein, mouseRecombinant Fusion ProteinsSmad3 ProteinSMAD3 protein, humanSMARCA4 protein, humanTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID21900401
PMCPMC3206175
OpenAlexW2039189450

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.