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CEBPA-dependent HK3 and KLF5 expression in primary AML and during AML differentiation

Academic Article
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Overview

authors

  • Federzoni, E. A.
  • Humbert, M.
  • Torbett, Bruce
  • Behre, G.
  • Fey, M. F.
  • Tschan, M. P.

publication date

  • March 2014

journal

  • Scientific Reports  Journal

abstract

  • The basic leucine zipper transcription factor CCAAT/enhancer binding protein alpha (CEBPA) codes for a critical regulator during neutrophil differentiation. Aberrant expression or function of this protein contributes to the development of acute myeloid leukemia (AML). In this study, we identified two novel unrelated CEBPA target genes, the glycolytic enzyme hexokinase 3 (HK3) and the krüppel-like factor 5 (KLF5) transcription factor, by comparing gene profiles in two cohorts of CEBPA wild-type and mutant AML patients. In addition, we found CEBPA-dependent activation of HK3 and KLF5 transcription during all-trans retinoic acid (ATRA) mediated neutrophil differentiation of acute promyelocytic leukemia (APL) cells. Moreover, we observed direct regulation of HK3 by CEBPA, whereas our data suggest an indirect regulation of KLF5 by this transcription factor. Altogether, our data provide an explanation for low HK3 and KLF5 expression in particular AML subtype and establish these genes as novel CEBPA targets during neutrophil differentiation.

subject areas

  • CCAAT-Enhancer-Binding Proteins
  • Cell Differentiation
  • Cell Line, Tumor
  • Cell Transformation, Neoplastic
  • Hexokinase
  • Humans
  • Kruppel-Like Transcription Factors
  • Leukemia, Myeloid, Acute
  • Neutrophils
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Identity

PubMed Central ID

  • PMC3939455

International Standard Serial Number (ISSN)

  • 2045-2322

Digital Object Identifier (DOI)

  • 10.1038/srep04261

PubMed ID

  • 24584857
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Additional Document Info

start page

  • 4261

volume

  • 4

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