Differential gene expression analysis of pediatric acute myeloid leukemia cell lines treated with azacytidine and panobinostat alone or in combination and compared to vehicle treated cells.
Pediatric AML cell lines (MV4;11, AML-193 and THP-1) were treated with DNA hypomethylating agent (azacytidine) and a pan histone deactylase inhibitor (panobinostat) alone or in combination. Treatment of AML cell lines with these epigenetic drugs synergistically suppresses cell viability in vitro and in xenograft models in vivo. Data show differential regulation of gene expression in AML cell lines by epigenetic drugs at concentrations which retained cell viability at a minimum of 75% even in the combination treatment.
Overall design
MV4;11 cells were treated with vehicle (0.1% DMSO), 0.5 uM azacytidine, 1.5 nM panobinostat or 0.5 uM azacytidine + 1.5 nM panobinostat for 48 h. AML-193 cells were treated with vehicle (0.1% DMSO), 5 uM azacytidine, 5 nM panobinostat or 5 uM azacytidine + 5 nM panobinostat for 48 h. THP-1 cells were treated with vehicle (0.1% DMSO), 3 uM azacytidine, 5 nM panobinostat or 3 uM azacytidine + 5 nM panobinostat for 48 h
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