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Sox4 Is a Key Oncogenic Target in C/EBP alpha Mutant Acute Myeloid Leukemia
- Zhang, Hong (author)
- Alberich-Jorda, Meritxell (author)
- Amabile, Giovanni (author)
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- Yang, Henry (author)
- Staber, Philipp B. (author)
- DiRuscio, Annalisa (author)
- Welner, Robert S. (author)
- Ebralidze, Alexander (author)
- Zhang, Junyan (author)
- Levantini, Elena (author)
- Lefebvre, Veronique (author)
- Valk, Peter J. M. (author)
- Delwel, Ruud (author)
- Hoogenkamp, Maarten (author)
- Nerlov, Claus (author)
- Saez, Borja (author)
- Scadden, David T. (author)
- Bonifer, Constanze (author)
- Ye, Min (author)
- Tenen, Daniel G. (author)
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- (creator_code:org_t)
- Elsevier BV, 2013
- 2013
- English.
- In: Cancer Cell. - : Elsevier BV. - 1878-3686 .- 1535-6108. ; 24:5, s. 575-588
- Journal article (peer-reviewed)
Abstract
Subject headings
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- 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.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Cancer and Oncology (hsv//eng)
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