Fig. 4

Co-treatment with chidamide and ventoclax disrupts DNA damage response and results in DNA damage in MM cells. 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 DNA damage was detected by Comet assay. 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 used to analyze the expressions of γH2A.X, p-ATM, p-ATR, p-CHK1, p-CHK2, Rad51 and KU80. C Protein levels of γH2A.X, p-ATM, p-ATR, p-CHK1, p-CHK2, Rad51 and KU80 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)