Fig.5

BTK inhibitors reduced CYLD phosphorylation and enhanced apoptosis induced by rituximab of non-GCB-DLBC. a, b OCI-Ly10 (a) and HBL-1 (b) cells were treated with DMSO, 50 μg/ml rituximab, 10 μM PCI-32765, 10 μM ACP-196, combination of 50 μg/ml rituximab and 10 μM PCI-32765, combination of 50 μg/ml rituximab and 10 μM ACP-196 for 72 h, cell viability was detected by CellTiter-Glo assay. c, d OCI-Ly10 (c) and HBL-1 (d) cells were treated with the same conditions as a and b, NFκB p65 subunit activation was measured by ELISA. e OCI-Ly10 cells were treated with 50 μg/ml rituximab, 10 μM. PCI-32765, 50 μg/ml rituximab + 10 μM PCI-32765 for 48 h, respectively. The apoptotic cell population including early and late apoptosis cells was quantified using an ApoDETECT Annexin V-FITC Kit and analyzed by flow cytometry. f Bars indicate the frequency of apoptotic OCI-Ly10 cell population including early and late apoptosis cells. g OCI-Ly10 cells were treated with 10 μM PCI-32765 or 10 μM ACP-196, with or without 50 μg/ml rituximab for 48 h, lysates were blotted with the indicated antibodies. The ATP level for each cell line treated with DMSO was set at 100%. The bars represent the mean ± SD from three independent experiments. *P < 0.05, **P < 0.01