Fig. 5: Cabozantinib inhibits AML1-ETO-mediated transcriptome.
From: Repurposing cabozantinib with therapeutic potential in KIT-driven t(8;21) acute myeloid leukaemias
A Western blot analysis of the phosphorylation of S6K and 4E-BP1. β-actin was loaded as a control. Signal intensity was quantified with ImageJ and normalised to β-actin and DMSO controls. B GSEA analysis identified genes upregulated following cabozantinib treatment were similar to a pre-defined gene set (DUNNE_TARGETS_OF_AML1_MTG8_FUSION_UP) comprising genes upregulated in Kasumi-1 cells after AML1-ETO knockdown by siRNA. C Relative mRNA expression of AML1-ETO-suppressed genes related to cell differentiation was analysed following 24-h of cabozantinib treatment in Kasumi-1 cells. Actin served as the internal control. Transcript levels were normalised to those of actin and the relative mRNA expression was calculated using the 2−ΔΔCT method. Each column represented the averages SD of three independent experiments (n = 3). ***p < 0.001, **p < 0.01, *p < 0.05, compared with DMSO control.
