ReviewAntioxidants & redox signaling2015
Class I HDACs Affect DNA Replication, Repair, and Chromatin Structure: Implications for Cancer Therapy.
Review in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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
33 citing papers in PubMed, 60 citations in OpenAlex.
- Chidamide inhibits the NOTCH1-MYC signaling axis in T-cell acute lymphoblastic leukemia.Frontiers of medicine · 2022Trial
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- DUSP26: Unveiling a critical molecular mediator and therapeutic target in developmental dysplasia of the hip‑associated secondary osteoarthritis.International journal of molecular medicine · 2026Article
- Preclinical Characterization of SDFZ-8, a Highly Potent HDAC1 Inhibitor, for Cancer Immunotherapy.MedComm · 2025Article
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Structural Modifications and Prospects of Histone Deacetylase (HDAC) Inhibitors in Cancer.Current medicinal chemistry · 2025Review
- Structure-Based Identification of Novel Histone Deacetylase 4 (HDAC4) Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2024Article
- CYLD induces high oxidative stress and DNA damage through class I HDACs to promote radiosensitivity in nasopharyngeal carcinoma.Cell death & disease · 2024Article
- Reversion from basal histone H4 hypoacetylation at the replication fork increases DNA damage in FANCA deficient cells.PloS one · 2024Article
- Differential histone deacetylase inhibitor-induced perturbations of the global proteome landscape in the setting of high-grade serous ovarian cancer.Proteomics · 2023Article
- Article
- 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
- BCL-3 loss sensitises colorectal cancer cells to DNA damage by targeting homologous recombination.DNA repair · 2022Article
- Predict long-range enhancer regulation based on protein-protein interactions between transcription factors.Nucleic acids research · 2021Article
- Entinostat, a selective HDAC1/2 inhibitor, potentiates the effects of olaparib in homologous recombination proficient ovarian cancer.Gynecologic oncology · 2021Article
- FK228 sensitizes radioresistant small cell lung cancer cells to radiation.Clinical epigenetics · 2021Article
- Article
- Adiponectin Deficiency Suppresses Rhabdomyosarcoma Associated with Gut Microbiota Regulation.BioMed research international · 2021Article
- Review
- PROTAC-mediated degradation of class I histone deacetylase enzymes in corepressor complexes.Chemical communications (Cambridge, England) · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
significanceThe contribution of epigenetic alterations to cancer development and progression is becoming increasingly clear, prompting the development of epigenetic therapies. Histone deacetylase inhibitors (HDIs) represent one of the first classes of such therapy. Two HDIs, Vorinostat and Romidepsin, are broad-spectrum inhibitors that target multiple histone deacetylases (HDACs) and are FDA approved for the treatment of cutaneous T-cell lymphoma. However, the mechanism of action and the basis for the cancer-selective effects of these inhibitors are still unclear. RECENT ADVANCES: While the anti-tumor effects of HDIs have traditionally been attributed to their ability to modify gene expression after the accumulation of histone acetylation, recent studies have identified the effects of HDACs on DNA replication, DNA repair, and genome stability. In addition, the HDIs available in the clinic target multiple HDACs, making it difficult to assign either their anti-tumor effects or their associated toxicities to the inhibition of a single protein. However, recent studies in mouse models provide insights into the tissue-specific functions of individual HDACs and their involvement in mediating the effects of HDI therapy. CRITICAL ISSUES: Here, we describe how altered replication contributes to the efficacy of HDAC-targeted therapies as well as discuss what knowledge mouse models have provided to our understanding of the specific functions of class I HDACs, their potential involvement in tumorigenesis, and how their disruption may contribute to toxicities associated with HDI treatment. FUTURE DIRECTIONS: Impairment of DNA replication by HDIs has important therapeutic implications. Future studies should assess how best to exploit these findings for therapeutic gain.
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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.