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Fig. 3 | Clinical Epigenetics

Fig. 3

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. 3

The potent pan-HDAC inhibitor MAKV-8 displays cytotoxic properties in CML cells. The acetylation levels of HDAC targets were assessed by western blot in K-562 cells treated with (a) increasing MAKV-8 concentrations for 24h or (b) 15µM MAKV-8 for the indicated time points. (c) CML cell proliferation and viability were evaluated following treatments with increasing MAKV-8 concentrations for up to 72h. (d) CML cells were grown in the presence of increasing MAKV-8 concentrations for 10 days, and their colony-forming capacity was scored after MTT addition. Representative pictures (left panel) and corresponding quantifications (right panel) from three independent experiments are provided. (e) Histone H4 and α-tubulin acetylation levels were assessed by western blot in KBM-5 and MEG-01 cells treated with increasing MAKV-8 concentrations for 24h. β-actin and histone H1 served as loading controls for α-tubulin and histone H4, respectively. Blots are representative of three independent experiments. SAHA was used as a reference HDACi

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