Fig. 5
Proscillaridin A Treatment Induces Downregulation of KATs Involved In MYC Acetylation. a KAT2A (GCN5), KAT3A (CBP), KAT3B (P300), KAT5 (TIP60), and KAT6A (MOZ) expression levels after proscillaridin A treatment (5 nM, 48 h) were assessed by western blotting in MOLT-4 cells (ACTIN was used as loading control). b Quantification of H3 acetylation levels after treatment with KAT3B/A inhibitor C646 (10 μM, 48 h) (* indicates P < 0.05; Two-way ANOVA; n = 3). c MYC protein expression after C646 treatment and proscillaridin A treatment (5 nM; 48 h). ACTIN was used as loading control. d MOLT-4, NALM-6, SW48 and A549 cell lines were treated with proscillaridin A (5 nM, 48 h) and fibroblasts transduced with RASV12, MYC and RASV12/MYC were treated with proscillaridin A (70 nM, 48 h). KAT3A (CBP), KAT3B (P300), KAT5 (TIP60), KAT2A (GCN5), KAT2B (PCAF), KAT6A (MOZ) and KAT7 (HBO1) expression levels were assessed by western blotting, quantified and expressed as percentage of untreated cells (* indicates P < 0.05; One-way ANOVA; n = 3). e Scheme showing that proscillaridin A targets high MYC expressing leukemic cells by inhibiting histone acetyltransferases involved in MYC acetylation and stability and causing loss of histone 3 acetylation