Journal of Nippon Medical School: Vol.69 No.3 page.224

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ArticleTitle Anti-tumor Effect of N-[3,4-dimethoxycinnamoyl]-anthranilic Acid (tranilast) on Experimental Pancreatic Cancer

AuthorList Makoto Hiroi, Masahiko Onda, Eiji Uchida, Takayuki Aimoto

Affiliation First Department of Surgery, Nippon Medical School

Language EN

Volume 69

Issue 3

Year 2002

Page 224-234

Received December 7, 2001

Accepted December 25, 2001

Keywords tranilast, hamster pancreatic cancer, proliferation, angiogenesis

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/m l (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/m l (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.

Correspondence to Makoto Hiroi, First Department of Surgery, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan
hiroi-surg1@nms.ac.jp

ArticleTitle	Anti-tumor Effect of N-[3,4-dimethoxycinnamoyl]-anthranilic Acid (tranilast) on Experimental Pancreatic Cancer
AuthorList	Makoto Hiroi, Masahiko Onda, Eiji Uchida, Takayuki Aimoto
Affiliation	First Department of Surgery, Nippon Medical School
Language	EN
Volume	69
Issue	3
Year	2002
Page	224-234
Received	December 7, 2001
Accepted	December 25, 2001
Keywords	tranilast, hamster pancreatic cancer, proliferation, angiogenesis
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/m l (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/m l (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.
Correspondence to	Makoto Hiroi, First Department of Surgery, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan hiroi-surg1@nms.ac.jp