RUNX1-ETO depletion in t(8;21) AML leads to C/EBPα- and AP-1-mediated alterations in enhancer-promoter interaction
Acute myeloid leukemia (AML) is associated with mutations in transcriptional and epigenetic regulator genes impairing myeloid differentiation. The t(8;21)(q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoietic master regulator RUNX1. We previously show...
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| Hauptverfasser: | , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
November 5, 2019
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| In: |
Cell reports
Year: 2019, Jahrgang: 28, Heft: 12, Pages: 3022–3031, e1–e7 |
| ISSN: | 2211-1247 |
| DOI: | 10.1016/j.celrep.2019.08.040 |
| Online-Zugang: | Verlag, Volltext: https://doi.org/10.1016/j.celrep.2019.08.040 Verlag: http://www.sciencedirect.com/science/article/pii/S2211124719310800 
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| Verfasserangaben: | Anetta Ptasinska, Anna Pickin, Salam A. Assi, Paulynn Suyin Chin, Luke Ames, Roberto Avellino, Stefan Gröschel, Ruud Delwel, Peter N. Cockerill, Cameron S. Osborne, and Constanze Bonifer |
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| 245 | 1 | 0 | |a RUNX1-ETO depletion in t(8;21) AML leads to C/EBPα- and AP-1-mediated alterations in enhancer-promoter interaction |c Anetta Ptasinska, Anna Pickin, Salam A. Assi, Paulynn Suyin Chin, Luke Ames, Roberto Avellino, Stefan Gröschel, Ruud Delwel, Peter N. Cockerill, Cameron S. Osborne, and Constanze Bonifer |
| 246 | 3 | 3 | |a RUNXone-ETO depletion in t(eight;twentyone) AML leads to C/EBPalpha- and AP-one-mediated alterations in enhancer-promoter interaction |
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| 520 | |a Acute myeloid leukemia (AML) is associated with mutations in transcriptional and epigenetic regulator genes impairing myeloid differentiation. The t(8;21)(q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoietic master regulator RUNX1. We previously showed that the maintenance of t(8;21) AML is dependent on RUNX1-ETO expression. Its depletion causes extensive changes in transcription factor binding, as well as gene expression, and initiates myeloid differentiation. However, how these processes are connected within a gene regulatory network is unclear. To address this question, we performed Promoter-Capture Hi-C assays, with or without RUNX1-ETO depletion and assigned interacting cis-regulatory elements to their respective genes. To construct a RUNX1-ETO-dependent gene regulatory network maintaining AML, we integrated cis-regulatory element interactions with gene expression and transcription factor binding data. This analysis shows that RUNX1-ETO participates in cis-regulatory element interactions. However, differential interactions following RUNX1-ETO depletion are driven by alterations in the binding of RUNX1-ETO-regulated transcription factors. | ||
| 650 | 4 | |a acute myeloid leukemia | |
| 650 | 4 | |a AP-1 signaling in acute myeloid leukemia | |
| 650 | 4 | |a chromatin programming | |
| 650 | 4 | |a epigenetic regulation | |
| 650 | 4 | |a integrated analysis of high-throughput data | |
| 650 | 4 | |a Promoter-Capture Hi-C | |
| 650 | 4 | |a promoter-enhancer interactions | |
| 650 | 4 | |a RUNX1-ETO | |
| 650 | 4 | |a transcription factors | |
| 650 | 4 | |a transcriptional networks | |
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