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Fig. 3 | Clinical Epigenetics

Fig. 3

From: The anticancer effects of MPT0G211, a novel HDAC6 inhibitor, combined with chemotherapeutic agents in human acute leukemia cells

Fig. 3

MPT0G211 potentiates doxorubicin-induced cytotoxicity by increasing apoptosis and decreasing DNA repair machinery in HL-60 cells. a The levels of the apoptotic proteins caspase 3 and poly-ADP ribose polymerase (PARP) and the pro-survival proteins BCL-XL, BCL-2, and survivin were determined in cells treated with MPT0G211 (3 μM) or tubastatin A (TBA) (3 μM) in combination with doxorubicin (DOXO) (0.1 μM) for 24 h. b Co-treatment of MPT0G211 or TBA with DOXO increased the phosphorylation of ATM, ATR, and CHK1 proteins. c The cells were incubated with MPT0G211 or TBA plus DOXO for 24 h, after which total cell lysates were immunoprecipitated with an anti-acetyl-lysine antibody and immunoblotted for Ku70. d Nuclear Ku70 protein levels were measured in cells treated with MPT0G211 or TBA in combination with DOXO. e Cells were incubated with MPT0G211 or TBA plus DOXO for 36 h, after which total cell lysates were immunoprecipitated with an anti-BAX antibody and immunoblotted for Ku70. f Cellular distributions of cytochrome c and BAX after co-treatment with MPT0G211 or TBA plus DOXO. g Antitumor activity of MPT0G211 plus doxorubicin in a HL-60 xenograft model. When the tumor size reached 200 mm3, mice were injected with vehicle, doxorubicin (1 mg/kg, i.p., q3d), and MPT0G211 (30 mg/kg, i.p., qd) alone or a combination of both. The curves of tumor growth volume were expressed as mean ± SEM. h Changes of body weight after treatment

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