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. 2014 Dec 2;6(1):185–195. doi: 10.18632/oncotarget.2688

Figure 1. C98 inhibits PI3K activity.

Figure 1

(A) Chemical structure of C98. (B) OPM2 cells were starved overnight and then treated with six compounds identified from the virtual screening for 2 hr, followed by IGF-1 stimulation for 15 min. Cell lysates were prepared for AKT expression and phosphorylation analyses. The known PI3K inhibitor S14161 was used as a positive control. (C) OPM2 cells were starved overnight, then treated with C98 at indicated concentration (25, 50 and 100 μM) or S14161 (100 μM) for 2 hr, followed by IGF-1 (100 ng/mL) stimulation for 15 min Cell lysates were prepared for AKT expression and phosphorylation analyses. (D) OPM2 cells were starved overnight and then treated with C98 (100 μM) for the indicated time periods (0.5, 1, 2 hr) or S14161 (100 μM) for 2 hr, followed by treatment with 100 ng/mL of IGF-1 for 15 min Cell lysates were prepared for AKT expression and phosphorylation analyses. (E) PI3K activity analyses in a cell-free system. Increasing concentrations of C98 were incubated with the recombinant PI3K isoforms α, β, δ, and γ, respectively. Activity of each kinase was determined with HotSpot technology as described in the Methods section “Kinase activity in cell-free assay”.