Abstract
The anti-tumor effect of N- [3,4-dimethoxycinnamoyl] -anthranilic acid (tranilast) was examined in experimental pancreatic cancer. Proliferation of PGHAM-1 cells was inhibited by tranilast in a dose-dependent manner, showing a significant difference at a concentration of 25 μg/ml (p<0.05). In colony formation, tranilast reduced the number of colonies at a concentration of 25 μg/ml (p<0.01). DNA synthesis for 12 hours was attenuated dose-dependently and a significant difference was observed at concentrations of greater than 50 μg/ml (p<0.05). From cell cycle analysis, a dose-dependent increase in the distribution of G0-G1 phase was observed. In the dorsal air sac model, the mean angiogenesis indices in PGHAM-1 chambers were 4.17 ± 0.22 (control group) and 2.33 ± 0.84 (treatment group), and in VEGF chambers they were 3.60 ± 0.67 (control group) and 1.92 ± 0.42 (treatment group), In the peritoneal dissemination model, the quantity of sanguineous ascites, the number and the size of diaphragmatic nodules and the microvessel density (MVD) of the metastatic site were reduced by tranilast significantly. In conclusion, the anti-tumor effect of tranilast on proliferation and on tumor-angiogenesis was confirmed in experimental pancreatic cancer.
