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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Heart failure drug proscillaridin A targets MYC overexpressing leukemia through global loss of lysine acetylation

Fig. 3

Gene Reprogramming Induced by Proscillaridin A Is Associated with Global Acetylation Loss in Histone H3. a Left panel, MOLT-4 cells were treated with proscillaridin A (5 nM) and histones were acid-extracted after 8, 16, 24, 48, 72 and 96 h. Histone 3 acetylation levels were assessed using antibodies against K9 ac, K14 ac, K18 ac, K27 ac, and total histone 3 acetylation. H3 was used as loading control. Right panel, H3 acetylation levels at 48 h treatment were quantified and expressed as a percentage of untreated cells (* indicates P < 0.05; Two-way ANOVA; n = 3). b 2169 genes are marked by H3K27ac in promoter regions (− 500/+ 500 bp) in untreated MOLT-4 cells. RPKM values of differentially expressed genes (FC > 1; FC < -0.5) from RNA-sequencing data before and after proscillaridin A treatment are displayed (* indicates P < 0.006; paired t-test; n = 3). c Pie chart shows percentage of upregulated (black) and downregulated (grey, including 30 MYC targets) genes after treatment (5 nM, 48 h) of genes marked by H3K27ac and MYC binding in promoters of untreated MOLT-4 cells. d Metascape analysis of genes marked by H3K27ac in promoters in untreated MOLT-4 cells and downregulated after proscillaridin A treatment (5 nM; 48 h). Top 9 GO pathways are displayed. e Metascape analysis of the 30 MYC target genes

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