ArticleNature communications2019
ARID1A and PI3-kinase pathway mutations in the endometrium drive epithelial transdifferentiation and collective invasion.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
What it found
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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.
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Who cites it
83 citing papers in PubMed, 135 citations in OpenAlex.
- Gene mutant dosage is associated with prognosis and metastatic tropism in 60,000 clinical cancer samples.Nature genetics · 2026Article
- ARID1A loss drives gastric signet ring cell carcinoma by regulating mucin production and secretion.Nature communications · 2026Article
- Review
- ARID1A deficiency reprograms the tumor secretome, enhancing microenvironmental remodeling and metastatic dissemination in endometrial carcinoma.Cell death & disease · 2026Article
- The features and prognostic value of ARID1A mutation and protein expression in endometrial cancer of no specific molecular profile (NSMP) subtype: a retrospective study in a large Chinese cohort.Journal of cancer research and clinical oncology · 2026Article
- Inhibition of PRMT5 triggers synthetic lethality in ARID1A-deficient endometrial cancer by promoting aberrant R-loop accumulation.Molecular cancer · 2026Article
- MicroRNA Expression Profile in Endometriosis and Endometriosis-Associated Ovarian Cancer-Systematic Review.Cells · 2026Review
- Therapeutic targeting of interleukin-17C signaling in carcinogenesis of endometriosis.Cell reports. Medicine · 2025Article
- A multimodal knowledge-enhanced whole-slide pathology foundation model.Nature communications · 2025Article
- Shifted assembly and function of mSWI/SNF family subcomplexes underlie targetable dependencies in dedifferentiated endometrial carcinomas.Nature genetics · 2025Article
- Shifted assembly and function of mSWI/SNF family subcomplexes underlie targetable dependencies in dedifferentiated endometrial carcinomas.bioRxiv : the preprint server for biology · 2025Article
- ARID1A: gene, protein, and function in endometrial cancer.Oncogene · 2025Review
- Insights into the Molecular Mechanisms and Signaling Pathways of Epithelial to Mesenchymal Transition (EMT) in the Pathophysiology of Endometriosis.International journal of molecular sciences · 2025Review
- ARID1A and Its Impact Across the Hallmarks of Cancer.International journal of molecular sciences · 2025Review
- Article
- Nanoceria as a non-steroidal anti-inflammatory drug for endometriosis theranostics.Journal of controlled release : official journal of the Controlled Release Society · 2025Article
- Generation and characterization of a mouse model of conditional Chd4 knockout in the endometrial epithelium.PloS one · 2025Article
- Research Advances in Adenomyosis-Related Signaling Pathways and Promising Targets.Biomolecules · 2024Review
- ARID1A-BAF coordinates ZIC2 genomic occupancy for epithelial-to-mesenchymal transition in cranial neural crest specification.American journal of human genetics · 2024Article
- Organismal metabolism regulates the expansion of oncogenic PIK3CA mutant clones in normal esophagus.Nature genetics · 2024Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
ARID1A and PI3-Kinase (PI3K) pathway alterations are common in neoplasms originating from the uterine endometrium. Here we show that monoallelic loss of ARID1A in the mouse endometrial epithelium is sufficient for vaginal bleeding when combined with PI3K activation. Sorted mutant epithelial cells display gene expression and promoter chromatin signatures associated with epithelial-to-mesenchymal transition (EMT). We further show that ARID1A is bound to promoters with open chromatin, but ARID1A loss leads to increased promoter chromatin accessibility and the expression of EMT genes. PI3K activation partially rescues the mesenchymal phenotypes driven by ARID1A loss through antagonism of ARID1A target gene expression, resulting in partial EMT and invasion. We propose that ARID1A normally maintains endometrial epithelial cell identity by repressing mesenchymal cell fates, and that coexistent ARID1A and PI3K mutations promote epithelial transdifferentiation and collective invasion. Broadly, our findings support a role for collective epithelial invasion in the spread of abnormal endometrial tissue.
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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.