ArticleBlood cancer journal2015
The SUV39H1 inhibitor chaetocin induces differentiation and shows synergistic cytotoxicity with other epigenetic drugs in acute myeloid leukemia cells.
Article in Blood cancer journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 94 citations in OpenAlex.
- Inhibition of SUV39H1 as a potent therapeutic target in multiple myeloma.Haematologica · 2026Article
- Role of Histone Modifications and miRNA Regulations in the Toxicity of Trichloroethylene in Terms of Cell Cycle Regulation in Human Kidney Cells.Journal of applied toxicology : JAT · 2026Article
- The Trajectory of Epigenetic Chromatin Remodeling in Cardiometabolic Disease and its Therapeutic Implications.Journal of cardiovascular translational research · 2026Review
- LCP2 mediates SUV39H1-driven cellular senescence-related chemoresistance in natural killer/T-cell lymphoma.Cell death & disease · 2026Article
- p53 regulates the expression of histone modifiers to restrict stemness and maintain differentiated luminal identity in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- SUV39H1 maintains cancer stem cell chromatin state and properties in glioblastoma.JCI insight · 2025Article
- Significance of targeting DNMT3A mutations in AML.Annals of hematology · 2025Review
- SUV39H1 Regulates Gastric Cancer Progression via the H3K9me3/ALDOB Axis.Cell biochemistry and biophysics · 2025Article
- Triple Combination of Entinostat, a Bromodomain Inhibitor, and Cisplatin Is a Promising Treatment Option for Bladder Cancer.Cancers · 2024Article
- Chemical Genetics inACS chemical biology · 2024Article
- Chaetocin-mediated SUV39H1 inhibition targets stemness and oncogenic networks of diffuse midline gliomas and synergizes with ONC201.Neuro-oncology · 2024Article
- Epigenetic regulation as a therapeutic target in the malaria parasite Plasmodium falciparum.Malaria journal · 2024Review
- The Wnt-pathway corepressor TLE3 interacts with the histone methyltransferase KMT1A to inhibit differentiation in Rhabdomyosarcoma.Oncogene · 2024Article
- 2,5-Diketopiperazines (DKPs): Promising Scaffolds for Anticancer Agents.Current pharmaceutical design · 2024Review
- Epidrugs as Promising Tools to EliminatePharmaceutics · 2023Article
- Phytochemicals and bioactive compounds effective against acute myeloid leukemia: A systematic review.Food science & nutrition · 2023Article
- Article
- Impact of Histone Modifications and Their Therapeutic Targeting in Hematological Malignancies.International journal of molecular sciences · 2022Review
- H3K9 dimethylation safeguards cancer cells against activation of the interferon pathway.Science advances · 2022Article
- Fast H3K9 methylation promoted by CXCL12 contributes to nuclear changes and invasiveness of T-acute lymphoblastic leukemia cells.Oncogene · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigenetic modifying enzymes have a crucial role in the pathogenesis of acute myeloid leukemia (AML). Methylation of lysine 9 on histone H3 by the methyltransferase G9a and SUV39H1 is associated with inhibition of tumor suppressor genes. We studied the effect of G9a and SUV39H1 inhibitors on viability and differentiation of AML cells and tested the cytotoxicity induced by combination of G9a and SUV39H1 inhibitors and various epigenetic drugs. The SUV39H1 inhibitor (chaetocin) and the G9a inhibitor (UNC0638) caused cell death in AML cells at high concentrations. However, only chaetocin-induced CD11b expression and differentiation of AML cells at non-cytotoxic concentration. HL-60 and KG-1a cells were more sensitive to chaetocin than U937 cells. Long-term incubation of chaetocin led to downregulation of SUV39H1 and reduction of H3K9 tri-methylation in HL-60 and KG-1a cells. Combination of chaetocin with suberoylanilide hydroxamic acid (SAHA, a histone deacetylase inhibitor) or JQ (a BET (bromodomain extra terminal) bromodomain inhibitor) showed synergistic cytotoxicity. Conversely, no synergism was found by combining chaetocin and UNC0638. More importantly, chaetocin-induced differentiation and combined cytotoxicity were also found in the primary cells of AML patients. Collectively, the SUV39H1 inhibitor chaetocin alone or in combination with other epigenetic drugs may be effective for the treatment of AML.
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