Figure 5
Inhibition of HDAC rescues MCSFR and GMCSFR expression in AML cells that express lineage-specifying TFs and contain mutated or translocated RUNX1. Kasumi-1 cells contain RUNX1-ETO. CG-SH cells contain mutated RUNX1 and normal cytogenetics. (A) AML cells containing abnormal RUNX1 express high levels of the lineage-specifying TFs PU.1 and CEBPA. Western blot 72 hours after addition of drug. (B-C) Treatment with HDAC inhibitors significantly increased MCSFR and GMCSFR mRNA and protein expression. Kasumi-1 and CG-SH were treated once with SAHA 1μM or MS-275 0.5μM. mRNA expression was measured by quantitative RT-PCR 72 hours after HDAC inhibitor treatment. Data are mean ± SD. HDAC inhibitor treatment versus vehicle treatment: *P < .05, **P < .01 (Student t test). Protein expression was measured by flow cytometry. Experiments were performed in triplicate.

Inhibition of HDAC rescues MCSFR and GMCSFR expression in AML cells that express lineage-specifying TFs and contain mutated or translocated RUNX1. Kasumi-1 cells contain RUNX1-ETO. CG-SH cells contain mutated RUNX1 and normal cytogenetics. (A) AML cells containing abnormal RUNX1 express high levels of the lineage-specifying TFs PU.1 and CEBPA. Western blot 72 hours after addition of drug. (B-C) Treatment with HDAC inhibitors significantly increased MCSFR and GMCSFR mRNA and protein expression. Kasumi-1 and CG-SH were treated once with SAHA 1μM or MS-275 0.5μM. mRNA expression was measured by quantitative RT-PCR 72 hours after HDAC inhibitor treatment. Data are mean ± SD. HDAC inhibitor treatment versus vehicle treatment: *P < .05, **P < .01 (Student t test). Protein expression was measured by flow cytometry. Experiments were performed in triplicate.

Close Modal

or Create an Account

Close Modal
Close Modal