Expression data from PU.1low URE-/- AML cell line after treatment with small molecule acting as PU.1 inhibitor. Mus musculus

Downregulation of the hematopoietic transcription factor PU.1 in PU.1 low acute myeloid leukemia cells (AML) by novel heterocyclic diamidines or PU.1 inhibitors leads to decrease cell proliferation and apoptosis, representing a new therapeutic strategy for AML treatment. These inhibitors induces decreased PU.1 binding on its target sites, as well as deregulation in PU.1 canonical target genes We used microarray to identify the pathways deregulated after drug treatment. Overall design: We treated PU.1low URE-/- AML cell line, derived from an URE-/- mouse at leukemic stage, with Vehicle (H2O) or PU.1 inhibitor (DB2313) during 24h. After cell collection and RNA extraction, samples were hybridized on Affymetrix microarrays.