ArticleCell reports2022
Arid1a mutation suppresses TGF-β signaling and induces cholangiocarcinoma.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Development and Validation of a Crotonylation-Related Prognostic Risk Model for Cholangiocarcinoma Based on Integrative Transcriptome Analysis.Digestive diseases and sciences · 2026Article
- ARID1A loss drives gastric signet ring cell carcinoma by regulating mucin production and secretion.Nature communications · 2026Article
- Identification of prognostic markers related to homologous recombination deficiency in cholangiocarcinoma using CoxBoost and LASSO machine learning techniques.Frontiers in immunology · 2026Article
- PTEN status on gonadotropin-releasing hormone (GnRH) metabolite, GnRH-(1-5), effects in endometrial cancer cell lines migration, & transcriptomic analysis of basal cell line and tumor gene expressions†.Biology of reproduction · 2025Article
- Molecular Alterations and Pathways in Intrahepatic Cholangiocarcinoma: Available Evidence and New Perspectives.International journal of molecular sciences · 2025Review
- Chronic Liver Disease Associated Cholangiocarcinoma: Genomic Insights and Precision Therapeutic Strategies.Cancers · 2025Review
- ARID1A: gene, protein, and function in endometrial cancer.Oncogene · 2025Review
- IDH Mutant Cholangiocarcinoma: Pathogenesis, Management, and Future Therapies.Current oncology (Toronto, Ont.) · 2025Review
- AMDHD1 acts as a tumor suppressor and contributes to activation of TGF-β signaling pathway in cholangiocarcinoma.Cell death and differentiation · 2025Article
- Opening and changing: mammalian SWI/SNF complexes in organ development and carcinogenesis.Open biology · 2024Review
- PRDM3/16 regulate chromatin accessibility required for NKX2-1 mediated alveolar epithelial differentiation and function.Nature communications · 2024Article
- A cuproptosis-related gene expression signature predicting clinical prognosis and immune responses in intrahepatic cholangiocarcinoma detected by single-cell RNA sequence analysis.Cancer cell international · 2024Article
- Multiomics analysis reveals metabolic subtypes and identifies diacylglycerol kinase α (DGKA) as a potential therapeutic target for intrahepatic cholangiocarcinoma.Cancer communications (London, England) · 2024Article
- ARID1A loss induces P4HB to activate fibroblasts to support lung cancer cell growth, invasion, and chemoresistance.Cancer science · 2024Article
- Targeting mTOR signaling for the treatment of intrahepatic cholangiocarcinoma with TSC1/ARID1A mutations: a case report with an unexpected response.Therapeutic advances in medical oncology · 2024Article
- PRDM3/16 Regulate Chromatin Accessibility Required for NKX2-1 Mediated Alveolar Epithelial Differentiation and Function.bioRxiv : the preprint server for biology · 2023Article
- Review
- Heterozygous Knockout ofGenes · 2023Article
- Review
- The Role of Genetic Mutations in Mitochondrial-Driven Cancer Growth in Selected Tumors: Breast and Gynecological Malignancies.Life (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Activating KRAS mutations and functional loss of members of the SWI/SNF complex, including ARID1A, are found together in the primary liver tumor cholangiocarcinoma (CC). How these mutations cooperate to promote CC has not been established. Using murine models of hepatocyte and biliary-specific lineage tracing, we show that Kras and Arid1a mutations drive the formation of CC and tumor precursors from the biliary compartment, which are accelerated by liver inflammation. Using cultured cells, we find that Arid1a loss causes cellular proliferation, escape from cell-cycle control, senescence, and widespread changes in chromatin structure. Notably, we show that the biliary proliferative response elicited by Kras/Arid1a cooperation and tissue injury in CC is caused by failed engagement of the TGF-β-Smad4 tumor suppressor pathway. We thus identify an ARID1A-TGF-β-Smad4 axis as essential in limiting the biliary epithelial response to oncogenic insults, while its loss leads to biliary pre-neoplasia and CC.
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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.