ArticleNature cell biology2017
ARID1A-mutated ovarian cancers depend on HDAC6 activity.
Article in Nature cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers.
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Who cites it
158 citing papers in PubMed, 224 citations in OpenAlex.
- Epigenetic mechanisms and clinical translation in ovarian cancer: from molecular pathways to precision therapy.Bioscience reports · 2026Review
- Histone Deacetylase Meets Protein Degradation: Accelerating Anticancer Drug Discovery.Medicinal research reviews · 2026Review
- Acetylation in ovarian cancer: mechanistic insights into drug resistance and emerging therapeutic opportunities.Journal of ovarian research · 2026Review
- Differential DNA damage response to WRN inhibition identifies a targetable vulnerability inScience advances · 2026Article
- Protein modification systems as cancer biomarkers and therapeutic targets.Precision clinical medicine · 2026Review
- Integration of gene expression profiling and mutation analysis via RNA sequencing: transitioning the 95-gene classifier to a next-generation platform in early-stage HR+/HER2- breast cancer.Breast cancer (Tokyo, Japan) · 2026Article
- SETD8 promotes ovarian clear cell carcinoma by epigenetically activating RNA metabolism genes via H4K20me1.Scientific reports · 2026Article
- Article
- Natural Compounds as Epimodulators in Epithelial Ovarian Cancer.Epigenomes · 2026Review
- Targeting miR-4653-3p/SLC25A51/SIRT3 axis to induce synthetic lethality in ARID1A-deficient colorectal cancer via blockade of DNA repair.Journal of translational medicine · 2026Article
- Epigenetics in Ovarian Cancer: A Review of Current Knowledge and Future Perspectives.Biomedicines · 2025Review
- Establishment of novel cholangiocarcinoma cell lines with ARID1A deficiency and preclinical validation of synthetic lethality therapies.Scientific reports · 2025Article
- ARID1A loss enhances sensitivity to c-MET inhibition by dual targeting of GPX4 and iron homeostasis, inducing ferroptosis.Cell death and differentiation · 2025Article
- Selective Alanine Transporter Utilization Is a Therapeutic Vulnerability in ARID1A-Mutant Ovarian Cancer.Cancer research · 2025Article
- Article
- The -124C>T Mutation of theCurrent oncology (Toronto, Ont.) · 2025Article
- Arid1a deficiency sensitises pancreatic cancer to fatty acid synthase inhibition.Clinical and translational medicine · 2025Article
- ARID1A deficiency promotes malignant proliferation of hepatocellular carcinoma by activating HDAC7/ENO1 signaling pathway.Hepatology communications · 2025Article
- ARID1A and Its Impact Across the Hallmarks of Cancer.International journal of molecular sciences · 2025Review
- Article
98 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
ARID1A, encoding a subunit of the SWI/SNF chromatin-remodelling complex, is the most frequently mutated epigenetic regulator across all human cancers. ARID1A and TP53 mutations are typically mutually exclusive. Therapeutic approaches that correlate with this genetic characteristic remain to be explored. Here, we show that HDAC6 activity is essential in ARID1A-mutated ovarian cancers. Inhibition of HDAC6 activity using a clinically applicable small-molecule inhibitor significantly improved the survival of mice bearing ARID1A-mutated tumours. This correlated with the suppression of growth and dissemination of ARID1A-mutated, but not wild-type, tumours. The dependence on HDAC6 activity in ARID1A-mutated cells correlated with a direct transcriptional repression of HDAC6 by ARID1A. HDAC6 inhibition selectively promoted apoptosis of ARID1A-mutated cells. HDAC6 directly deacetylates Lys120 of p53, a pro-apoptotic post-translational modification. Thus, ARID1A mutation inactivates the apoptosis-promoting function of p53 by upregulating HDAC6. Together, these results indicate that pharmacological inhibition of HDAC6 is a therapeutic strategy for ARID1A-mutated cancers.
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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.