Journal
CANCER CELL
Volume 24, Issue 5, Pages 575-588Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2013.09.018
Keywords
-
Categories
Funding
- National Institutes of Health [HL 56745, CA118316, NIH/NIAMS R01 AR54153]
- Harvard Stem Cell Institute [DP-0086-10-00]
- Navrat grant from the Czech Ministry of Youth, Health and Sports [LK21307]
- Collegio Ghislieri fellowship
- Austrian Research Foundation
- European Union
- Societa' Italiana di Ematologia Sperimentale borsa di studio
- Jose Carreras Leukemia Foundation [FIJC F11/01]
- FAMRI CIA
- Leukaemia Lymphoma Research
- Medical Research Council [G0902418, G0900892] Funding Source: researchfish
- MRC [G0902418, G0900892] Funding Source: UKRI
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available