ArticleNucleic acids research2024
ARID1A regulates DNA repair through chromatin organization and its deficiency triggers DNA damage-mediated anti-tumor immune response.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular and Clinicopathological Biomarkers Predicting Brain Metastasis in Triple-Negative Breast Cancer: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Targeting the DNA Damage Response in Cancer.MedComm · 2026Review
- The dual immune landscape of homologous recombination-deficient tumors: mechanisms and therapeutic implications.Cancer metastasis reviews · 2026Review
- Deacetylase-independent HDAC1 condensation defines temozolomide response in glioblastoma.Nature chemical biology · 2026Article
- The roles of chromatin remodeling and 3D genome organization in cancers: from mechanistic insights to emerging treatment options.Molecular cancer · 2026Review
- ID3 deficiency alters chromatin accessibility at DSB sites and enhances vulnerability to HDAC inhibition.International journal of cancer · 2026Article
- Epigenetic modulation of prostate cancer disparities in men with African ancestry.Nature reviews. Urology · 2026Review
- DNA damage response signature-based prognostic genes for intrahepatic cholangiocarcinoma: a combined analysis of machine learning and biological experiments.Cancer cell international · 2026Article
- Molecular convergence in gallbladder cancer: MEK-ERK signalling at the crossroads of oncogenic hubs and pathway cross-talks.Cancer cell international · 2026Review
- Neoantigen Targeting as a Novel Approach for Therapy-Resistant Tumors.Molecular diagnosis & therapy · 2026Review
- Two-year treatment-free sustained remission after chemo-immunotherapy in a 52-year-old male with recurrentTranslational lung cancer research · 2026Article
- Chromatin Remodeling, DNA Double-Strand Break Repair, and Human Disease: How a Breakup Changes You.Biomolecules · 2026Review
- Article
- Twenty-four months progression-free survival (ongoing) for treatment of recurrent ovarian clear cell carcinoma with surufatinib in combination with toripalimab: a case report.BMC women's health · 2026Article
- Micronuclei: origins, assays, mechanisms, diseases and treatments.Signal transduction and targeted therapy · 2026Review
- Subtyping atypical eosinophilic renal cell tumours through integrated morphological, immunohistochemical, and mutational characters.BMC cancer · 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
- Article
- Targeting WEE1 in ARID1A/TP53 Concurrent Mutant Colorectal Cancer by Exploiting R-Loop Accumulation and DNA Repair Deficiencies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Conserved 3D genome reorganization during DNA repair.Life science alliance · 2026Review
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19 authors.
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Abstract
AT-rich interaction domain protein 1A (ARID1A), a SWI/SNF chromatin remodeling complex subunit, is frequently mutated across various cancer entities. Loss of ARID1A leads to DNA repair defects. Here, we show that ARID1A plays epigenetic roles to promote both DNA double-strand breaks (DSBs) repair pathways, non-homologous end-joining (NHEJ) and homologous recombination (HR). ARID1A is accumulated at DSBs after DNA damage and regulates chromatin loops formation by recruiting RAD21 and CTCF to DSBs. Simultaneously, ARID1A facilitates transcription silencing at DSBs in transcriptionally active chromatin by recruiting HDAC1 and RSF1 to control the distribution of activating histone marks, chromatin accessibility, and eviction of RNAPII. ARID1A depletion resulted in enhanced accumulation of micronuclei, activation of cGAS-STING pathway, and an increased expression of immunomodulatory cytokines upon ionizing radiation. Furthermore, low ARID1A expression in cancer patients receiving radiotherapy was associated with higher infiltration of several immune cells. The high mutation rate of ARID1A in various cancer types highlights its clinical relevance as a promising biomarker that correlates with the level of immune regulatory cytokines and estimates the levels of tumor-infiltrating immune cells, which can predict the response to the combination of radio- and immunotherapy.
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