A metabolic interplay coordinated by HLX regulates myeloid differentiation and AML through partly overlapping pathways View Full Text


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Article Info

DATE

2018-12

AUTHORS

Indre Piragyte, Thomas Clapes, Aikaterini Polyzou, Ramon I. Klein Geltink, Stylianos Lefkopoulos, Na Yin, Pierre Cauchy, Jonathan D. Curtis, Lhéanna Klaeylé, Xavier Langa, Cora C. A. Beckmann, Marcin W. Wlodarski, Patrick Müller, Dominic Van Essen, Angelika Rambold, Friedrich G. Kapp, Marina Mione, Joerg M. Buescher, Erika L. Pearce, Alexander Polyzos, Eirini Trompouki

ABSTRACT

The H2.0-like homeobox transcription factor (HLX) regulates hematopoietic differentiation and is overexpressed in Acute Myeloid Leukemia (AML), but the mechanisms underlying these functions remain unclear. We demonstrate here that HLX overexpression leads to a myeloid differentiation block both in zebrafish and human hematopoietic stem and progenitor cells (HSPCs). We show that HLX overexpression leads to downregulation of genes encoding electron transport chain (ETC) components and upregulation of PPARδ gene expression in zebrafish and human HSPCs. HLX overexpression also results in AMPK activation. Pharmacological modulation of PPARδ signaling relieves the HLX-induced myeloid differentiation block and rescues HSPC loss upon HLX knockdown but it has no effect on AML cell lines. In contrast, AMPK inhibition results in reduced viability of AML cell lines, but minimally affects myeloid progenitors. This newly described role of HLX in regulating the metabolic state of hematopoietic cells may have important therapeutic implications. More... »

PAGES

3090

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-018-05311-4

    DOI

    http://dx.doi.org/10.1038/s41467-018-05311-4

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1105928842

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30082823


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