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Effect of ZFX shRNA mediated knockdown in the human AML cell line NOMO-1

ABSTRACT: Acute myeloid leukemia (AML) and acute T-lymphoblastic leukemia (T-ALL) maintain the undifferentiated phenotype and proliferative capacity of their respective cells of origin, hematopoietic stem/progenitor cells and immature thymocytes. The mechanisms that maintain these progenitor-like characteristics are poorly understood. We report that the transcription factor Zfx is required for the development and propagation of experimental AML caused by MLL-AF9 fusion, and of T-ALL caused by Notch1 activation. In both leukemia types, Zfx activated progenitor-associated gene expression programs and prevented differentiation. Key Zfx target genes included mitochondrial enzymes Ptpmt1 and Idh2, whose overexpression partially rescued the propagation of Zfx-deficient AML. These studies identify a common mechanism that controls the cell-of-origin characteristics of acute leukemias derived from disparate lineages and transformation mechanisms. NOMO-1 cells were infected with control and ZFX shRNA lentiviruses at an MOI of 1. RNA was collected for microarrays 48 hours after selection.

ORGANISM(S): Homo sapiens  

SUBMITTER: Boris V Reizis   Stuart P Weisberg  Stuart Weisberg 

PROVIDER: E-GEOD-43021 | ArrayExpress | 2015-01-01



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