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Fig. 12 | Clinical Epigenetics

Fig. 12

From: Novel HDAC inhibitor MAKV-8 and imatinib synergistically kill chronic myeloid leukemia cells via inhibition of BCR-ABL/MYC-signaling: effect on imatinib resistance and stem cells

Fig. 12

Altered BCR-ABL signaling and autophagy induction are associated with MAKV-8-imatinib anti-cancer properties. CML cells were treated with the indicated concentrations of imatinib alone or in combination with MAKV-8. (a, b) K-562 cells were transfected with or without the indicated siRNA, then (a) the expression level of beclin-1, a protein involved in initiating the autophagic flux, was assessed by western blot 24 and 72h post-transfection, and (b) nuclear morphology (upper panel) and PARP-1 cleavage (lower panel) were analyzed in cells treated for 24 and 48h, respectively. The ratio between the cleaved and uncleaved forms of PARP-1 was determined based on western blot quantification. (c, d) Protein expression and phosphorylation levels were assessed by western blot in cells treated for 24h. Blots used β-actin as a loading control and are representative of three independent experiments. SAHA was used as a reference HDACi

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