Počet záznamů: 1
Sox4 is a key oncogenic target in C/EBP alpha mutant acute myeloid leukemia
- 1.0422959 - ÚMG 2014 RIV US eng J - Článek v odborném periodiku
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
Grant CEP: GA MŠMT LK21307
Institucionální podpora: RVO:68378050
Klíčová slova: Sox4 * C/EBP alpha * acute myeloid leukemia
Kód oboru RIV: EB - Genetika a molekulární biologie
Impakt faktor: 23.893, rok: 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.
Trvalý link: http://hdl.handle.net/11104/0229176
Počet záznamů: 1