ArticlePloS one2013
A histone acetyltransferase p300 inhibitor C646 induces cell cycle arrest and apoptosis selectively in AML1-ETO-positive AML cells.
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 54 papers.
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Who cites it
54 citing papers in PubMed, 100 citations in OpenAlex.
- The role of epigenetic modifications in hematological cancers.Frontiers in oncology · 2026Review
- Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 2026Review
- EP300 compromises antitumor immunity by increasing SOCS1 expression.Journal for immunotherapy of cancer · 2025Article
- Gene regulatory complexes: their role and regulation across normal and malignant hematopoiesis.Experimental hematology · 2025Review
- t(8;21)AML patients with RUNX1e6::RUNX1T19a splice variant have poor prognosis.Annals of hematology · 2025Article
- Protein lactylation and immunotherapy in gliomas: A novel regulatory axis in tumor metabolism (Review).International journal of oncology · 2025Review
- Development of C646-Based Proteolysis Targeting Chimeras Degraders of the Lysine Acetyltransferases CBP and p300.ChemMedChem · 2025Article
- The ESCRT protein CHMP5 promotes T cell leukemia by enabling BRD4-p300-dependent transcription.Nature communications · 2025Article
- Epigenetic dynamics in meniscus cell migration and its zonal dependency in response to inflammatory conditions.APL bioengineering · 2025Article
- Exploring epigenetic strategies for the treatment of osteoporosis.Molecular biology reports · 2024Review
- Luteotropic and Luteolytic Factors Modulate the Expression of Nuclear Receptor Coregulators in Bovine Luteal Cells Independently of Histone Acetyltransferase and Histone Deacetylase Activities.Animals : an open access journal from MDPI · 2023Article
- Effects of the Acetyltransferase p300 on Tumour Regulation from the Novel Perspective of Posttranslational Protein Modification.Biomolecules · 2023Review
- Molecular characterization of the histone acetyltransferase CREBBP/EP300 genes in myeloid neoplasia.Leukemia · 2022Article
- Recent advances in epigenetic anticancer therapeutics and future perspectives.Frontiers in genetics · 2022Review
- Adipocyte-mediated epigenomic instability in human T-ALL cells is cytotoxic and phenocopied by epigenetic-modifying drugs.Frontiers in cell and developmental biology · 2022Article
- p300 suppresses the transition of myelodysplastic syndromes to acute myeloid leukemia.JCI insight · 2021Article
- C646 inhibits G2/M cell cycle-related proteins and potentiates anti-tumor effects in pancreatic cancer.Scientific reports · 2021Article
- Protein Acetylation at the Interface of Genetics, Epigenetics and Environment in Cancer.Metabolites · 2021Review
- Effects of the histone acetylase inhibitor C646 on growth and differentiation of adipose-derived stem cells.Cell cycle (Georgetown, Tex.) · 2021Article
- p300 is upregulated by docetaxel and is a target in chemoresistant prostate cancer.Endocrine-related cancer · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AML1-ETO fusion protein (AE) is generated by t(8;21)(q22;q22) chromosomal translocation, which is one of the most frequently observed structural abnormalities in acute myeloid leukemia (AML) and displays a pivotal role in leukemogenesis. The histone acetyltransferase p300 promotes self-renewal of leukemia cells by acetylating AE and facilitating its downstream gene expression as a transcriptional coactivator, suggesting that p300 may be a potential therapeutic target for AE-positive AML. However, the effects of p300 inhibitors on leukemia cells and the underlying mechanisms have not been extensively investigated. In the current study, we analyzed the anti-leukemia effects of C646, a selective and competitive p300 inhibitor, on AML cells. Results showed that C646 inhibited cellular proliferation, reduced colony formation, evoked partial cell cycle arrest in G1 phase, and induced apoptosis in AE-positive AML cell lines and primary blasts isolated from leukemic mice and AML patients. Nevertheless, no significant inhibitory effects were observed in granulocyte colony-stimulating factor-mobilized normal peripheral blood stem cells. Notably, AE-positive AML cells were more sensitive to lower C646 doses than AE-negative ones. And C646-induced growth inhibition on AE-positive AML cells was associated with reduced global histone H3 acetylation and declined c-kit and bcl-2 levels. Therefore, C646 may be a potential candidate for treating AE-positive AML.
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