Figure 5
C646 induces apoptosis of pancreatic cancer cells. Effects of C646 on apoptosis (A)/(B) and therapeutic efficacy of C646 treatment against pancreatic tumors transplanted in nude mice (C)/(D). (A) Cancer cells were treated with C646 at 30 µM for 48 h and fixed in 70% ethanol at − 20 °C overnight. Fixed cells were stained with for annexin V-FITC and propidium iodide. The proportions of apoptotic cells were significantly increased as C646 concentration was increased, compared with the control cells. Error bars represent mean ± SD. *p < 0.05 vs controls. (B) Cancer cells were treated with C646 at 30 µM for 48 h. The expression of apoptotic markers was increased by C646 treatment compared with controls. (C) Mice were inoculated with MIAPaCa2 cells in the flank by subcutaneous injection. Once tumors reached measurable size in 10 days, C646 (10 mg/kg) or vehicle (DMSO) were administrated by i.p. injection daily for two weeks. The dose of C646 was set to 10 mg/kg, which is the lower dose in this study, referring to previous literature47. The volume of the tumors in mice was recorded over for eight weeks (C646, vehicle, and nontreated; each N = 4). C646 treatment in pancreatic cancer suppressed the growth of the tumor significantly (*p < 0.01 by one-way ANOVA with post hoc Dunnett's test). Error bars represent mean ± SD. (D) Representative images of transplanted tumors in mice at the time of necropsy (left panel, vehicle; right panel, C646).
