Fig. 5

The JAK2/STAT3 pathway is involved in DCZ0858-mediated anti-tumor effects in the DLBCL cells. a The efficiency of JAK2 knockdown was verified by western blot analysis. b The efficiency of JAK2 overexpression was determined by western blotting. c OCI-LY8 and NU-DUL-1 cells were cotreated with JAK2 shRNAs and DCZ0858 (2.5–40 μM) for 48 h. CCK-8 assays were used to detect the inhibition rates at different DCZ0858 concentrations. d NU-DUL-1 and OCI-LY8 cells were cotreated with JAK2 shRNAs and DCZ0858 (40 μM) for 48 h, double-stained with annexin V-APC/7-AAD, and analyzed by flow cytometry. e Clone colonies formed by the OCI-LY8 and NU-DUL-1 cells cotreated with shJAK2-1 and DCZ0858 (40 μM); colonies in each well were quantified. f NU-DUL-1 and OCI-LY8 cells were cotreated with shJAK2-1 and DCZ0858 (40 μM) for 48 h and then protein levels were assessed by western blotting. g NU-DUL-1 and OCI-LY8 cells were pretreated with JAK2 inhibitor (ruxolitinib) for 2 h and then treated with DCZ0858 (40 μM) for 48 h. h NU-DUL-1 and OCI-LY8 cells were cotreated with JAK2-OE and DCZ0858 (40 μM) for 48 h, and analyzed by western blotting. i The efficiency of STAT3 knockdown and overexpression was verified by qRT-PCR. j The expression of c-Myc after treatment with DCZ0858. k The change in c-Myc expression after STAT3 overexpression and knockdown. l A schematic showing the involvement of JAK2/STAT3 in DCZ0858-mediated antitumor effects in the DLBCL cells. All data are presented as the means ± SD on the basis of triplicate measures; *P < 0.05, **P < 0.01, and #P < 0.05