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Carcinogenesis Advance Access originally published online on January 23, 2004
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Carcinogenesis, Vol. 25, No. 6, 979-985, June 2004
Carcinogenesis vol.25 no.6 © Oxford University Press 2004; all rights reserved.

ARTICLE

An acyclic retinoid, NIK-333, inhibits N-diethylnitrosamine-induced rat hepatocarcinogenesis through suppression of TGF-{alpha} expression and cell proliferation

Masataka Kagawa, Tetsuro Sano, Naoto Ishibashi, Manabu Hashimoto, Masataka Okuno1, Hisataka Moriwaki1, Rikako Suzuki2, Hiroyuki Kohno2 and Takuji Tanaka2,3

Pharmaceutical Research Laboratories, Nikken Chemicals Co. Ltd, 1-346 Kitabukuro-cho, Omiya-ku, Saitama-shi, Saitama 330-0835, 1 First Department of Internal Medicine, Gifu University School of Medicine, 40 Tsukasa-machi, Gifu 550-8705 and 2 First Department of Pathology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa 920-0293, Japan

3 To whom correspondence should be addressed Email: takutt{at}kanazawa-med.ac.jp

The present study was designed to determine the effects of NIK-333, a synthetic acyclic retinoid, on N-diethylnitrosamine (DEN)-induced hepatocarcinogenesis in male F344 rats. Animals were given DEN dissolved in drinking water at a concentration of 40 p.p.m. for 5 weeks and then provided with drinking water free of DEN for 15 weeks to induce hepatocellular neoplasms. NIK-333 was administered orally (once a day) to rats at doses of 10, 40 and 80 mg/kg body wt for 14 weeks, starting 1 week after the completion of administration of DEN. At 20 weeks after the start of DEN administration, histopathological evaluation was carried out on all animals. The effects of NIK-333 on the cell proliferation activity of non-tumorous areas and liver tumor cells and the immunohistochemical expression of transforming growth factor-{alpha} (TGF-{alpha}) were also evaluated. NIK-333 at 40 and 80 mg/kg body wt significantly inhibited hepatocarcinogenesis (P < 0.05). In addition, NIK-333 at the same doses decreased DEN-induced overexpression of TGF-{alpha} in hepatocellular neoplasms (adenomas and carcinomas) and their surrounding tissue. Furthermore, NIK-333 significantly inhibited cell proliferation activity in the lesions and in non-tumorous areas (P < 0.01). Our results suggest that NIK-333 inhibits DEN-induced hepatocarcinogenesis through suppression of TGF-{alpha} expression and cell proliferation.


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