ArticleCancer letters2017
Down-regulation of ARID1A is sufficient to initiate neoplastic transformation along with epigenetic reprogramming in non-tumorigenic endometriotic cells.
Article in Cancer letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- Comprehensive molecular characterization identifies therapeutic vulnerabilities in ovarian clear cell carcinoma.Genome medicine · 2026Article
- Article
- Therapeutic targeting of interleukin-17C signaling in carcinogenesis of endometriosis.Cell reports. Medicine · 2025Article
- ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5.BMC pulmonary medicine · 2025Article
- Mutation profile and molecular heterogeneity in mismatch repair deficient endometrial carcinoma.Frontiers in oncology · 2025Article
- Article
- The roles of chromatin regulatory factors in endometriosis.Journal of assisted reproduction and genetics · 2024Review
- Review
- The genomic and molecular landscape of splenic marginal zone lymphoma, biological and clinical implications.Exploration of targeted anti-tumor therapy · 2024Review
- (mis)-Targeting of SWI/SNF complex(es) in cancer.Cancer metastasis reviews · 2023Review
- Endothelial Arid1a deletion disrupts the balance among angiogenesis, neurogenesis and gliogenesis in the developing brain.Cell proliferation · 2023Article
- Cell-type dependent regulation of pluripotency and chromatin remodeling genes by hydralazine.Stem cell research & therapy · 2023Article
- The Emerging Role of Chromatin Remodeling Complexes in Ovarian Cancer.International journal of molecular sciences · 2022Review
- Treating ARID1A mutated cancers by harnessing synthetic lethality and DNA damage response.Journal of biomedical science · 2022Review
- Role of ARID1A in the Regulation of Human Trophoblast Migration and Invasion.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- GLS1 is a protective factor in patients with ovarian clear cell carcinoma and its expression does not correlate with ARID1A-mutated tumors.Cancer research communications · 2022Article
- Validated biomarker assays confirm that ARID1A loss is confounded with MMR deficiency, CD8The Journal of pathology · 2022Article
- Emerging Themes in Mechanisms of Tumorigenesis by SWI/SNF Subunit Mutation.Epigenetics insights · 2022Review
- The Evolutionary Conserved SWI/SNF Subunits ARID1A and ARID1B Are Key Modulators of Pluripotency and Cell-Fate Determination.Frontiers in cell and developmental biology · 2021Review
- ARID1A Mutations Promote P300-Dependent Endometrial Invasion through Super-Enhancer Hyperacetylation.Cell reports · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The chromatin remodeler AT-Rich Interactive Domain 1A (ARID1A) is frequently mutated in ovarian clear cell carcinoma (OCCC) and endometriosis precursor lesions. Here, we show that knocking down ARID1A in an immortalized endometriosis cell line is sufficient to induce phenotypic changes indicative of neoplastic transformation as evidenced by higher efficiency of anchorage-independent growth, increased propensity to adhere to collagen, and greater capacity to invade basement membrane extract in vitro. ARID1A knockdown is associated with expression dysregulation of 99 target genes, and many of these expression changes are also observed in primary OCCC tissues. Further, pathway analysis indicates these genes fall within networks highly relevant to tumorigenesis including integrin and paxillin pathways. We demonstrate that the down-regulation of ARID1A does not markedly alter global chromatin accessibility or DNA methylation but unexpectedly, we find strong increases in the active H3K27ac mark in promoter regions and decreases of H3K27ac at potential enhancers. Taken together, these data provide evidence that ARID1A mutation can be an early stage event in the oncogenic transformation of endometriosis cells giving rise to OCCC.
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Registered trials
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.