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

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    0422959 - ÚMG 2014 RIV US eng J - Journal Article
    Zhang, H. - Alberich-Jorda, Meritxell - Amabile, G. - Yang, H. - Staber, P.B. - DiRuscio, A. - Welner, R.S. - Ebralidze, A. - Zhang, J. - Levantini, E. - Lefebvre, V. - Valk, P.J. - Delwel, R. - Hoogenkamp, M. - Nerlov, C. - Cammenga, J. - Saez, B. - Scadden, D.T. - Bonifer, C. - Ye, M. - Tenen, D.G.
    Sox4 is a key oncogenic target in C/EBP alpha mutant acute myeloid leukemia.
    Cancer Cell. Roč. 24, č. 5 (2013), s. 575-588. ISSN 1535-6108. E-ISSN 1878-3686
    R&D Projects: GA MŠMT LK21307
    Institutional support: RVO:68378050
    Keywords : Sox4 * C/EBP alpha * acute myeloid leukemia
    Subject RIV: EB - Genetics ; Molecular Biology
    Impact factor: 23.893, year: 2013

    Mutation 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.
    Permanent Link: http://hdl.handle.net/11104/0229176

     
     
Number of the records: 1  

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