The Hematopoietic Transcription Factors RUNX1 and ERG Prevent AML1-ETO Oncogene Overexpression and Onset of the Apoptosis Program in t(8;21) AMLs

Amit Mandoli, Abhishek A. Singh, Koen H. M. Prange, Esther Tijchon, Marjolein Oerlemans, Rene Dirks, Menno Ter Huurne, Albertus T. J. Wierenga, Eva M. Janssen-Megens, Kim Berentsen, Nilofar Sharifi, Bowon Kim, Filomena Matarese, Luan N. Nguyen, Nina C. Hubner, Nagesha A. Rao, Emile van den Akker, Lucia Altucci, Edo Vellenga, Hendrik G. StunnenbergJoost H. A. Martens*

*Corresponding author for this work

    Research output: Contribution to journalArticleAcademicpeer-review

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    Abstract

    The t(8;21) acute myeloid leukemia (AML)-associated oncoprotein AML1-ETO disrupts normal hematopoietic differentiation. Here, we have investigated its effects on the transcriptome and epigenome in t(8,21) patient cells. AML1-ETO binding was found at promoter regions of active genes with high levels of histone acetylation but also at distal elements characterized by low acetylation levels and binding of the hematopoietic transcription factors LYL1 and LMO2. In contrast, ERG, FLI1, TAL1, and RUNX1 bind at all AML1-ETO-occupied regulatory regions, including those of the AML1-ETO gene itself, suggesting their involvement in regulating AML1-ETO expression levels. While expression of AML1-ETO in myeloid differentiated induced pluripotent stem cells (iPSCs) induces leukemic characteristics, overexpression increases cell death. We find that expression of wild-type transcription factors RUNX1 and ERG in AML is required to prevent this oncogene overexpression. Together our results show that the interplay of the epigenome and transcription factors prevents apoptosis in t(8;21) AML cells.

    Original languageEnglish
    Pages (from-to)2087-2100
    Number of pages14
    JournalCell reports
    Volume17
    Issue number8
    DOIs
    Publication statusPublished - 15-Nov-2016

    Keywords

    • ACUTE MYELOID-LEUKEMIA
    • PLURIPOTENT STEM-CELLS
    • SELF-RENEWAL
    • GENOME-WIDE
    • GRANULOCYTIC DIFFERENTIATION
    • DEFINITIVE HEMATOPOIESIS
    • GENE-EXPRESSION
    • HDAC INHIBITION
    • HISTONE H4
    • AML1/ETO

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