Evidence map›Paper›PMID 38873993›Full record

ArticleInternational journal of oncology2024

ARID1A restrains EMT and stemness of ovarian cancer cells through the Hippo pathway.

Shouying Xu, Chongying Zhu, Qiang Xu, Zihao An, Shu Xu, Ge Xuan, Chao Lin, Chao Tang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. ARID1A and Its Impact Across the Hallmarks of Cancer.International journal of molecular sciences · 2025
    Review
  11. Review
  12. Review
  13. GPR137-RAB8A activation promotes ovarian cancer development via the Hedgehog pathway.Journal of experimental & clinical cancer research : CR · 2025
    Article
  14. 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

8 authors.

Shouying XuNational Clinical Research Center for Child Health of the Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310052, P.R. China.
Chongying ZhuThe Department of Obstetrics and Gynecology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200025, P.R. China.
Qiang XuNational Clinical Research Center for Child Health of the Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310052, P.R. China.
Zihao AnNational Clinical Research Center for Child Health of the Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310052, P.R. China.
Shu XuNational Clinical Research Center for Child Health of the Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310052, P.R. China.
Ge XuanDepartment of Gynecology, Ningbo Women and Children's Hospital, Ningbo, Zhejiang 315012, P.R. China.
Chao LinDepartment of Neurosurgery, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310052, P.R. China.
Chao TangNational Clinical Research Center for Child Health of the Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310052, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genes encoding subunits of SWI/SNF (BAF) chromatin‑remodeling complexes are recurrently mutated in a broad array of tumor types, and among the subunits, ARID1A is the most frequent target with mutations. In the present study, it was reported that ARID1A inhibits the epithelial‑mesenchymal transition (EMT) and stemness of ovarian cancer cells, accompanied by reduced cell viability, migration and colony formation, suggesting that ARID1A acts as a tumor suppressor in ovarian cancer. Mechanistically, ARID1A exerts its inhibitory effects on ovarian cancer cells by activating the Hippo signaling pathway. Conversely, the overexpression of a gain‑of‑function transcriptional co‑activator with PDZ‑binding motif (TAZ) mutant (TAZ‑Ser89) effectively reverses the effects induced by ARID1A. In addition, activation of Hippo signaling apparently upregulates ARID1A protein expression, whereas ectopic expression of TAZ‑Ser89 results in the markedly decreased ARID1A levels, indicating a feedback of ARID1A‑TAZ in regulating ovarian cancer cell EMT and stemness. Thus, the present study uncovered the role of ARID1A through the Hippo/TAZ pathway in modulating EMT and stemness of ovarian cancer cells, and providing with evidence that TAZ inhibitors could effectively prevent initiation and metastasis of ovarian cancer cases where ARID1A is lost or mutated.

Indexed as

Epithelial-Mesenchymal TransitionHippo Signaling PathwayNeoplastic Stem CellsOvarian NeoplasmsTranscription FactorsCell Line, TumorCell MovementCell ProliferationDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticHumansNuclear ProteinsProtein Serine-Threonine KinasesSignal TransductionTranscriptional Coactivator with PDZ-Binding Motif ProteinsARID1A protein, humanDNA-Binding ProteinsNuclear ProteinsProtein Serine-Threonine KinasesTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsWWTR1 protein, humanAT‑rich interaction domain 1AHippoovarian cancerstemnesstranscriptional co‑activator with PDZ‑binding motif

Identifiers

PMID38873993
PMCPMC11251745

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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.