ArticleClinical cancer research : an official journal of the American Association for Cancer Research2016
HDAC Inhibition Induces MicroRNA-182, which Targets RAD51 and Impairs HR Repair to Sensitize Cells to Sapacitabine in Acute Myelogenous Leukemia.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 73 citations in OpenAlex.
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- miR-320a enhances radiosensitivity in non-small cell lung cancer by targeting RAD51 and modulating ferroptosis via GPX4.Scientific reports · 2026Article
- A potent dual inhibitor targeting COX-2 and HDAC of acute myeloid leukemia cells.Molecular diversity · 2025Article
- Repurposing Linezolid in Conjunction with Histone Deacetylase Inhibitor Access in the Realm of Glioblastoma Therapies.Journal of medicinal chemistry · 2025Article
- The potential synergistic effect of combining doxorubicin with vorinostat in urothelial carcinoma therapy.Heliyon · 2025Article
- Exosomal miR-92b-5p regulates N4BP1 to enhance PTEN mono-ubiquitination in doxorubicin-resistant AML.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- Dissecting the epigenetic orchestra of HDAC isoforms in breast cancer development: a review.Medical oncology (Northwood, London, England) · 2024Review
- Characterisation of miRNA Expression in Dental Pulp Cells during Epigenetically-Driven Reparative Processes.International journal of molecular sciences · 2023Article
- Multifaceted Influence of Histone Deacetylases on DNA Damage Repair: Implications for Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2023Review
- HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023Review
- Article
- Implication of microRNAs in Carcinogenesis with Emphasis on Hematological Malignancies and Clinical Translation.International journal of molecular sciences · 2022Review
- Disruption of DNA Repair and Survival Pathways through Heat Shock Protein Inhibition by Onalespib to Sensitize Malignant Gliomas to Chemoradiation Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Interactions between miRNAs and Double-Strand Breaks DNA Repair Genes, Pursuing a Fine-Tuning of Repair.International journal of molecular sciences · 2022Review
- The Emerging Roles of Rad51 in Cancer and Its Potential as a Therapeutic Target.Frontiers in oncology · 2022Review
- Vulnerability of IDH1-Mutant Cancers to Histone Deacetylase Inhibition via Orthogonal Suppression of DNA Repair.Molecular cancer research : MCR · 2021Article
- Footprints of microRNAs in Cancer Biology.Biomedicines · 2021Review
- Histone deacetylase 6 acts upstream of DNA damage response activation to support the survival of glioblastoma cells.Cell death & disease · 2021Article
- DNA damage repair: historical perspectives, mechanistic pathways and clinical translation for targeted cancer therapy.Signal transduction and targeted therapy · 2021Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe double-strand breaks elicited by sapacitabine, a clinically active nucleoside analogue prodrug, are repaired by RAD51 and the homologous recombination repair (HR) pathway, which could potentially limit its toxicity. We investigated the mechanism by which histone deacetylase (HDAC) inhibitors targeted RAD51 and HR to sensitize acute myelogenous leukemia (AML) cells to sapacitabine. EXPERIMENTAL
designChromatin immunoprecipitation identified the role of HDACs in silencing miR-182 in AML. Immunoblotting, gene expression, overexpression, or inhibition of miR-182 and luciferase assays established that miR-182 directly targeted RAD51. HR reporter assays, apoptotic assays, and colony-forming assays established that the miR-182, as well as the HDAC inhibition-mediated decreases in RAD51 inhibited HR repair and sensitized cells to sapacitabine.
resultsThe gene repressors, HDAC1 and HDAC2, became recruited to the promoter of miR-182 to silence its expression in AML. HDAC inhibition induced miR-182 in AML cell lines and primary AML blasts. miR-182 targeted RAD51 protein both in luciferase assays and in AML cells. Overexpression of miR-182, as well as HDAC inhibition-mediated induction of miR-182 were linked to time- and dose-dependent decreases in the levels of RAD51, an inhibition of HR, increased levels of residual damage, and decreased survival after exposure to double-strand damage-inducing agents.
conclusionsOur findings define the mechanism by which HDAC inhibition induces miR-182 to target RAD51 and highlights a novel pharmacologic strategy that compromises the ability of AML cells to conduct HR, thereby sensitizing AML cells to DNA-damaging agents that activate HR as a repair and potential resistance mechanism. Clin Cancer Res; 22(14); 3537-49. ©2016 AACR.
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