ArticleLeukemia2012
Chromatin modifications induced by the AML1-ETO fusion protein reversibly silence its genomic targets through AML1 and Sp1 binding motifs.
Article in Leukemia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Mitochondria and Their Relationship with Common Genetic Abnormalities in Hematologic Malignancies.Life (Basel, Switzerland) · 2021Review
- KDM4B promotes acute myeloid leukemia associated with AML1-ETO by regulating chromatin accessibility.FASEB bioAdvances · 2021Article
- AML1/ETO and its function as a regulator of gene transcription via epigenetic mechanisms.Oncogene · 2021Review
- RUNX1/RUNX1T1 mediates alternative splicing and reorganises the transcriptional landscape in leukemia.Nature communications · 2021Article
- Review
- Article
- Prognostic value of the PDLIM family in acute myeloid leukemia.American journal of translational research · 2019Article
- Allogeneic hematopoietic stem cell transplantation for relapsed acute myeloid leukemia in ETO positive with reduced-intensity conditioning.Oncotarget · 2018Article
- MYC-dependent recruitment of RUNX1 and GATA2 on the SET oncogene promoter enhances PP2A inactivation in acute myeloid leukemia.Oncotarget · 2017Article
- ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia.Nature communications · 2017Article
- Article
- AML1/ETO cooperates with HIF1α to promote leukemogenesis through DNMT3a transactivation.Leukemia · 2015Article
- Review
- Review
- AML1-ETO driven acute leukemia: insights into pathogenesis and potential therapeutic approaches.Frontiers of medicine · 2012Review
- Depletion of RUNX1/ETO in t(8;21) AML cells leads to genome-wide changes in chromatin structure and transcription factor binding.Leukemia · 2012Article
- Abrogation of RUNX1 gene expression in de novo myelodysplastic syndrome with t(4;21)(q21;q22).Haematologica · 2012Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
The AML1-ETO fusion protein, which is present in 10-15% of cases of acute myeloid leukemia, is known to repress myeloid differentiation genes through DNA binding and recruitment of chromatin-modifying proteins and transcription factors in target genes. ChIP-chip analysis of human hematopoietic stem/progenitor cells transduced with the AML1-ETO fusion gene enabled us to identify 1168 AML1-ETO target genes, 103 of which were co-occupied by histone deacetylase 1 (HDAC1) and had lost the hyperacetylation mark at histone H4, and 264 showed a K9 trimethylation at histone H3. Enrichment of genes involved in hematopoietic differentiation and in specific signaling pathways was observed in the presence of these epigenetic modifications associated with an 'inactive' chromatin status. Furthermore, AML1-ETO target genes had a significant correlation between the chromatin marks studied and transcriptional silencing. Interestingly, AML1 binding sites were absent on a large number of selected AML1-ETO promoters and an Sp1 binding site was found in over 50% of them. Reversible silencing induced by the fusion protein in the presence of AML1 and/or Sp1 transcription factor binding site was confirmed. Therefore, this study provides a global analysis of AML1-ETO functional chromatin modifications and identifies the important role of Sp1 in the DNA binding pattern of AML1-ETO, suggesting a role for Sp1-targeted therapy in this leukemia subtype.
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