ArticleCell reports2018
Repurposing Pan-HDAC Inhibitors for ARID1A-Mutated Ovarian Cancer.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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.
The trial behind it
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
70 citing papers in PubMed, 98 citations in OpenAlex.
- Evaluation of novel targeted small-molecule therapeutics in desmoplastic small round cell tumor (DSRCT) cells.Journal of cancer research and clinical oncology · 2026Article
- Overcoming Therapy Resistance in Ovarian Cancer: From Molecular Mechanisms to Emerging Therapeutic Strategies.Cancers · 2026Review
- Acetylation in ovarian cancer: mechanistic insights into drug resistance and emerging therapeutic opportunities.Journal of ovarian research · 2026Review
- Article
- Epigenetic regulation in early embryogenesis: mechanisms, developmental programming, and transgenerational implications.Frontiers in cell and developmental biology · 2026Review
- Epigenetics in Ovarian Cancer: A Review of Current Knowledge and Future Perspectives.Biomedicines · 2025Review
- A Comparative Analysis of Usual- and Gastric-Type Cervical Adenocarcinoma in a Japanese Population Reveals Distinct Clinicopathological and Molecular Features with Prognostic and Therapeutic Insights.International journal of molecular sciences · 2025Article
- miR-490-5p inhibits the progression of osteosarcoma by targeting HDAC2.Translational cancer research · 2025Article
- EZH2 inhibitor SHR2554 enhances the anti-tumor efficacy of HDAC inhibitor Chidamide through STAT1 in T-cell lymphoma.Cell death & disease · 2025Article
- Relationship between the protein expression of ARID1A, ARID1B and ARID2 with the clinicopathological characteristics of colorectal cancer.Biomedical reports · 2025Article
- High-Throughput Drug Screening of Clear Cell Ovarian Cancer Organoids Reveals Vulnerability to Proteasome Inhibitors and Dinaciclib and Identifies AGR2 as a Therapeutic Target.Cancer research communications · 2025Article
- Impaired ARID1A expression attenuated the immune response in gastric cancer via histone acetylation.Clinical epigenetics · 2025Article
- Chromatin remodeling complexes: architects influencing breast cancer progression.Frontiers in cell and developmental biology · 2025Review
- Uterine carcinosarcoma: Unraveling the role of epithelial-to-mesenchymal transition in progression and therapeutic potential.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- The PRC2 complex epigenetically silences GATA4 to suppress cellular senescence and promote the progression of breast cancer.Translational oncology · 2024Article
- The Histone Deacetylase Family: Structural Features and Application of Combined Computational Methods.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Hypoxia-activated XBP1s recruits HDAC2-EZH2 to engage epigenetic suppression of ΔNp63α expression and promote breast cancer metastasis independent of HIF1α.Cell death and differentiation · 2024Article
- From clinical management to personalized medicine: novel therapeutic approaches for ovarian clear cell cancer.Journal of ovarian research · 2024Review
- Targeting SWI/SNF Complexes in Cancer: Pharmacological Approaches and Implications.Epigenomes · 2024Review
- Therapeutic Role of Synthetic Lethality inJournal of immunotherapy and precision oncology · 2024Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
ARID1A, a subunit of the SWI/SNF complex, is among the most frequently mutated genes across cancer types. ARID1A is mutated in more than 50% of ovarian clear cell carcinomas (OCCCs), diseases that have no effective therapy. Here, we show that ARID1A mutation confers sensitivity to pan-HDAC inhibitors such as SAHA in ovarian cancers. This correlated with enhanced growth suppression induced by the inhibition of HDAC2 activity in ARID1A-mutated cells. HDAC2 interacts with EZH2 in an ARID1A status-dependent manner. HDAC2 functions as a co-repressor of EZH2 to suppress the expression of EZH2/ARID1A target tumor suppressor genes such as PIK3IP1 to inhibit proliferation and promote apoptosis. SAHA reduced the growth and ascites of the ARID1A-inactivated OCCCs in both orthotopic and genetic mouse models. This correlated with a significant improvement of survival of mice bearing ARID1A-mutated OCCCs. These findings provided preclinical rationales for repurposing FDA-approved pan-HDAC inhibitors for treating 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.