ArticleOncotarget2017
Histone deacetylases 1 and 2 cooperate in regulating BRCA1, CHK1, and RAD51 expression in acute myeloid leukemia cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Endothelial progenitor cell susceptibility to DNA damaging and DDR-modulating compounds determines endothelial differentiation accuracy.Stem cell research & therapy · 2026Article
- HDAC1/2-mediated deacetylation of KLF9 promotes the malignant progression of nasopharyngeal carcinoma via CDH17.Oncogene · 2025Article
- Acetylation of Steroidogenic Acute Regulatory Protein Sensitizes 17β-Estradiol Regulation in Hormone-Sensitive Breast Cancer Cells.International journal of molecular sciences · 2024Article
- A high-throughput approach to identify BRCA1-downregulating compounds to enhance PARP inhibitor sensitivity.iScience · 2024Article
- Epigenetic Dysregulation and Its Correlation with the Steroidogenic Machinery Impacting Breast Pathogenesis: Data Mining and Molecular Insights into Therapeutics.International journal of molecular sciences · 2023Article
- Therapeutic efficacy of an injectable formulation of purinostat mesylate in SU-DHL-6 tumour model.Annals of medicine · 2022Article
- VPA and TSA Interrupt the Interplay between mutp53 and HSP70, Leading to CHK1 and RAD51 Down-Regulation and Sensitizing Pancreatic Cancer Cells to AZD2461 PARP Inhibitor.International journal of molecular sciences · 2022Article
- Inhibitors of class I HDACs and of FLT3 combine synergistically against leukemia cells with mutant FLT3.Archives of toxicology · 2022Article
- Epigenetic Mechanisms in DNA Double Strand Break Repair: A Clinical Review.Frontiers in molecular biosciences · 2021Review
- The translational repressor 4E-BP1 regulates RRM2 levels and functions as a tumor suppressor in Ewing sarcoma tumors.Oncogene · 2021Article
- Small subset of Wnt-activated cells is an initiator of regrowth in colorectal cancer organoids after irradiation.Cancer science · 2020Article
- Regulating the Regulators: The Role of Histone Deacetylase 1 (HDAC1) in Erythropoiesis.International journal of molecular sciences · 2020Review
- PAICS contributes to gastric carcinogenesis and participates in DNA damage response by interacting with histone deacetylase 1/2.Cell death & disease · 2020Article
- In Vitro Assessment of the Genotoxic Hazard of Novel Hydroxamic Acid- and Benzamide-Type Histone Deacetylase Inhibitors (HDACi).International journal of molecular sciences · 2020Article
- Role of HDACs in normal and malignant hematopoiesis.Molecular cancer · 2020Review
- Safety and efficacy of oral panobinostat plus chemotherapy in patients aged 65 years or younger with high-risk acute myeloid leukemia.Leukemia research · 2019Article
- HDAC2-dependent miRNA signature in acute myeloid leukemia.FEBS letters · 2019Article
- Histone deacetylase 1 induced by neddylation inhibition contributes to drug resistance in acute myelogenous leukemia.Cell communication and signaling : CCS · 2019Article
- Targeting PI3K, mTOR, ERK, and Bcl-2 signaling network shows superior antileukemic activity against AML ex vivo.Biochemical pharmacology · 2018Article
- Vorinostat enhances the anticancer effect of oxaliplatin on hepatocellular carcinoma cells.Cancer medicine · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to chemotherapy and a high relapse rate highlight the importance of finding new therapeutic options for the treatment of acute myeloid leukemia (AML). Histone deacetylase (HDAC) inhibitors (HDACIs) are a promising class of drugs for the treatment of AML. HDACIs have limited single-agent clinical activities, but when combined with conventional or investigational drugs they have demonstrated favorable outcomes. Previous studies have shown that decreasing expression of important DNA damage repair proteins enhances standard chemotherapy drugs. In our recent studies, the pan-HDACI panobinostat has been shown to enhance conventional chemotherapy drugs cytarabine and daunorubicin in AML cells by decreasing the expression of BRCA1, CHK1, and RAD51. In this study, we utilized class- and isoform-specific HDACIs and shRNA knockdown of individual HDACs to determine which HDACs are responsible for decreased expression of BRCA1, CHK1, and RAD51 following pan-HDACI treatment in AML cells. We found that inhibition of both HDAC1 and HDAC2 was necessary to decrease the expression of BRCA1, CHK1, and RAD51, enhance cytarabine- or daunorubicin-induced DNA damage and apoptosis, and abrogate cytarabine- or daunorubicin-induced cell cycle checkpoint activation in AML cells. These findings may aid in the development of rationally designed drug combinations for the treatment of AML.
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