Fig. 3From: Chidamide and venetoclax synergistically exert cytotoxicity on multiple myeloma by upregulating BIM expressionCo-treatment with chidamide and venetoclax induces cell cycle arrest at the G0/G1 phase in HMCLs via activating P21 and P27. A HMCLs were incubated with chidamide (1ɥM for U266; 2ɥM for ARP-1 and MM1.S) and/or venetoclax (2ɥM for U266; 4ɥM for ARP-1 and MM1.S) for 48 h, and the cell cycle was analyzed by flow cytometry. B HMCLs were exposed to chidamide (1ɥM for U266; 2ɥM for ARP-1 and MM1.S) and/or venetoclax (2ɥM for U266; 4ɥM for ARP-1 and MM1.S) for 48 h. Western blotting was employed to detect the expression of the following cell cycle-related proteins: P21, P27, cyclin D1, cyclin E1, CDK4 and CDK6. C Protein levels of P21, P27, cyclin D1, cyclin E1, CDK4 and CDK6 were normalized to those of GAPDH and presented as fold changes relative to vehicle controls. Data are presented as the mean ± SD of at least three independent experiments. (ns P > 0.05; ∗ P < 0.05; ∗  ∗ P < 0.01; ***P < 0.001; ∗  ∗  ∗  ∗ P < 0.0001)Back to article page