Fig. 5: BRD9 inhibition enhances the antitumor effect of imatinib in vitro.

A GIST-882 cells were treated with GSK602 combined with imatinib at indicated concentration for 48 h. Cell viability was analyzed by MTT. B Combination index (CI) and fraction affected of GSK602 and imatinib combining at different concentration in GIST-882 cells treated for 48 h were analyzed by the CompuSyn program (ComboSyn). C GIST-T1 cells were treated with GSK602 combined with imatinib at indicated concentration for 48 h. Cell viability was analyzed by MTT. D Combination index (CI) and fraction affected of GSK602 and imatinib combining at different concentration in GIST-T1 cells treated for 48 h were analyzed by the CompuSyn program (ComboSyn). E Indicated cells were treated with 100 nM GSK602 and 50 nM imatinib for 24 h. The indicated proteins were analyzed by western blotting. F WT and PUMA-KO GIST-882 cells were treated with 100 nM GSK602 and 50 nM imatinib for 24 h. Apoptosis was analyzed by fragment nuclei assay. G WT and PUMA-KO GIST-T1 cells were treated with 100 nM GSK602 and 50 nM imatinib for 24 h. Apoptosis was analyzed by fragment nuclei assay. H WT and PUMA-KO GIST-882 or GIST-T1 cells were treated with the combination of 100 nM GSK602 and 50 nM imatinib for 24 h. Caspase 3 level was analyzed by western blotting. Results were expressed as means ± SD of three independent experiments. ***P < 0.001.