Number of the records: 1  

Sox4 is a key oncogenic target in C/EBP alpha mutant acute myeloid leukemia

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    SYSNO ASEP0422959
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleSox4 is a key oncogenic target in C/EBP alpha mutant acute myeloid leukemia
    Author(s) Zhang, H. (US)
    Alberich-Jorda, Meritxell (UMG-J) RID
    Amabile, G. (US)
    Yang, H. (SG)
    Staber, P.B. (US)
    DiRuscio, A. (US)
    Welner, R.S. (US)
    Ebralidze, A. (US)
    Zhang, J. (US)
    Levantini, E. (US)
    Lefebvre, V. (US)
    Valk, P.J. (NL)
    Delwel, R. (NL)
    Hoogenkamp, M. (GB)
    Nerlov, C. (GB)
    Cammenga, J. (SE)
    Saez, B. (US)
    Scadden, D.T. (US)
    Bonifer, C. (GB)
    Ye, M. (US)
    Tenen, D.G. (US)
    Source TitleCancer Cell. - : Elsevier - ISSN 1535-6108
    Roč. 24, č. 5 (2013), s. 575-588
    Number of pages14 s.
    Publication formPrint - P
    Languageeng - English
    CountryUS - United States
    KeywordsSox4 ; C/EBP alpha ; acute myeloid leukemia
    Subject RIVEB - Genetics ; Molecular Biology
    R&D ProjectsLK21307 GA MŠMT - Ministry of Education, Youth and Sports (MEYS)
    Institutional supportUMG-J - RVO:68378050
    UT WOS000327005100006
    DOI10.1016/j.ccr.2013.09.018
    AnnotationMutation or epigenetic silencing of the transcription factor C/EBP alpha is observed in similar to 10% of patients with acute myeloid leukemia (AML). In both cases, a common global gene expression profile is observed, but downstream targets relevant for leukemogenesis are not known. Here, we identify Sox4 as a direct target of C/EBP alpha whereby its expression is inversely correlated with C/EBP alpha activity. Downregulation of Sox4 abrogated increased self-renewal of leukemic cells and restored their differentiation. Gene expression profiles of leukemia-initiating cells (LICs) from both Sox4 overexpression and murine C/EBP alpha mutant AML models clustered together but differed from other types of AML. Our data demonstrate that Sox4 overexpression resulting from C/EBP alpha inactivation contributes to the development of leukemia with a distinct LIC phenotype.
    WorkplaceInstitute of Molecular Genetics
    ContactNikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217
    Year of Publishing2014
Number of the records: 1  

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