ArticlePloS one2013
Inhibition of histone deacetylase 3 causes replication stress in cutaneous T cell lymphoma.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 103 citations in OpenAlex.
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- Recommended Tool Compounds: Isoform- and Class-Specific Histone Deacetylase Inhibitors.ACS pharmacology & translational science · 2026Review
- HDAC3 inhibition as a therapeutic strategy in T-cell acute lymphoblastic leukemia via the TYK2-STAT1-BCL2 signaling pathway.Frontiers in immunology · 2026Article
- Combined HDAC and eIF4A inhibition: A novel epigenetic therapy for pancreatic ductal adenocarcinoma.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2026Article
- HDAC3 inhibitors induce drug resistance by promoting IL-17 A production by T cells.Scientific reports · 2024Article
- Novel hydroxamic acid derivative induces apoptosis and constrains autophagy in leukemic cells.Journal of advanced research · 2024Article
- Deficiency of histone deacetylases 3 in macrophage alleviates monosodium urate crystals-induced gouty inflammation in mice.Arthritis research & therapy · 2024Article
- Reversion from basal histone H4 hypoacetylation at the replication fork increases DNA damage in FANCA deficient cells.PloS one · 2024Article
- Article
- ATXN3 controls DNA replication and transcription by regulating chromatin structure.Nucleic acids research · 2023Article
- Cell-free circulating tumor RNAs in plasma as the potential prognostic biomarkers in colorectal cancer.Frontiers in oncology · 2023Article
- Targeting epigenetic regulators for inflammation: Mechanisms and intervention therapy.MedComm · 2022Review
- The Role of HDACs in the Response of Cancer Cells to Cellular Stress and the Potential for Therapeutic Intervention.International journal of molecular sciences · 2022Review
- Determination of Slow-Binding HDAC Inhibitor Potency and Subclass Selectivity.ACS medicinal chemistry letters · 2022Article
- Targeting Histone Deacetylases in Idiopathic Pulmonary Fibrosis: A Future Therapeutic Option.Cells · 2022Review
- Optimization of Class I Histone Deacetylase PROTACs Reveals that HDAC1/2 Degradation is Critical to Induce Apoptosis and Cell Arrest in Cancer Cells.Journal of medicinal chemistry · 2022Article
- High Histone Deacetylase 2/3 Expression in Non-Functioning Pituitary Tumors.Frontiers in oncology · 2022Article
- Dexmedetomidine inhibits mitochondria damage and apoptosis of enteric glial cells in experimental intestinal ischemia/reperfusion injury via SIRT3-dependent PINK1/HDAC3/p53 pathway.Journal of translational medicine · 2021Article
- Differential Effects of Histone Deacetylases on the Expression of NKG2D Ligands and NK Cell-Mediated Anticancer Immunity in Lung Cancer Cells.Molecules (Basel, Switzerland) · 2021Article
- Review
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
Abstract
Given the fundamental roles of histone deacetylases (HDACs) in the regulation of DNA repair, replication, transcription and chromatin structure, it is fitting that therapies targeting HDAC activities are now being explored as anti-cancer agents. In fact, two histone deacetylase inhibitors (HDIs), SAHA and Depsipeptide, are FDA approved for single-agent treatment of refractory cutaneous T cell lymphoma (CTCL). An important target of these HDIs, histone deacetylase 3 (HDAC3), regulates processes such as DNA repair, metabolism, and tumorigenesis through the regulation of chromatin structure and gene expression. Here we show that HDAC3 inhibition using a first in class selective inhibitor, RGFP966, resulted in decreased cell growth in CTCL cell lines due to increased apoptosis that was associated with DNA damage and impaired S phase progression. Through isolation of proteins on nascent DNA (iPOND), we found that HDAC3 was associated with chromatin and is present at and around DNA replication forks. DNA fiber labeling analysis showed that inhibition of HDAC3 resulted in a significant reduction in DNA replication fork velocity within the first hour of drug treatment. These results suggest that selective inhibition of HDAC3 could be useful in treatment of CTCL by disrupting DNA replication of the rapidly cycling tumor cells, ultimately leading to cell death.
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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.