Fig. 5
Co-exposure to chidamide and venetoclax induces apoptosis of HMCLs in connection with BIM upregulation. A 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. The expressions of the following BCL2 family proteins were determined by western blot analysis: BCL2, MCL1, BCL-XL and BIM. B Protein levels of BCL2, MCL1, BCL-XL and BIM were normalized to those of GAPDH and presented as fold changes relative to vehicle controls. C BCL-XL was knocked down by lentivirus in MM1.S cells. D BCL-XL was knocked down by lentivirus in U266 cells. E BIM was knocked down by lentivirus in ARP-1 cells. F BIM was knocked down by lentivirus in U266 cells. G MM1.S cells (upper) and U266 cells (down) with BCL-XL knockdown were treated with chidamide (2 μM) ± venetoclax (4 μM) for 48 h and the percentage of apoptosis was determined by flow cytometry H ARP-1 cells (upper) and U266 cells (down) with BIM knockdown were treated with chidamide (2 μM) ± venetoclax (4 μM for U266, 8 μM for ARP-1) for 48 h and the percentage of apoptosis was determined by flow cytometry (ns P > 0.05; ∗ P < 0.05; ∗  ∗ P < 0.01; ∗  ∗  ∗ P < 0.001; ∗  ∗  ∗  ∗ P < 0.0001)