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. 2017 Apr 10;8(25):41026–41043. doi: 10.18632/oncotarget.17010

Figure 7. The PDE3 inhibitor cilostazol reduced GIST882 viability and synergized with STI-571.

Figure 7

(A) WST-1 viability assay. GIST882 were treated with a concentration range of cilostazol for 24h, 48h and 72h prior to addition of WST-1 reagent. Cell viability reduction was time and concentration dependent. (B) GIST882 were treated with forskolin (0 to 100μM), cilostazol (0 to 10μM) and combination of the two at a 1:10 ratio (e.g: 1.25μM cilostazol+ 12.5μM forskolin) for 72h. (C) GIST882 were treated with STI-571 (0 to 2.5μM), cilostazol (0 to 5μM) and combination of the two at a 1:2 ratio (e.g: 0.5 μM STI-571 + cilostazol 1μM) for 72h. (D) Table shows calculated IC50 for cilostazol, forskolin and STI-571 and their respective dose reduction index (DRI). The CI50 value of 0.20 and 0.15 indicates synergism of cilostazol with forskolin and with STI-571, respectively, on cell viability reduction. #(Chou-Talalay's Combination Index for 50% of the effect). Mean values from five independent experiments. Data presented as mean +/- SEM. P-value (2 way ANOVA and Tukey's post- test) *: p {less than or equal to} 0.05. (E) Left panel: Western blot of GIST882 cells treated for 72h with STI-571 (1μM), cilostazol (10μM) and STI-571+cilostazol (1μM:10μM) probed with anti-pERK, anti-total ERK and anti-GAPDH. 100μg protein/lane. Right panel: pERK levels were significantly reduced in STI-571 and STI-571+cilostazol conditions. Data presented as mean +/- SEM. P-values (Kruskal-Wallis followed by Dunn's test). *: p {less than or equal to} 0.05.