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Canventol Inhibits Tumor Promotion in CD-1 Mouse Skin through Inhibition of Tumor Necrosis Factor Release and of Protein Isoprenylation¹

Cancer Prevention Division, National Cancer Center Research Institute, Tokyo 104, Japan [A. K., M. S., S. O., H. F.]. and Department of Chemistry, University of Hawaii at Manoa, Honolulu, Hawaii 96822 [X. Z. M. A. T.]

A synthetic compound named canventol, 2-isopropyl-4-isopropyl-idenecyclohex-2-ene-1-o1, inhibited tumor promotion of okadaic acid on mouse skin initiated with 7,12-dimethylbenz(a)anthracene in two-stage carcinogenesis experiments more strongly than sarcophytol A, isolated from a soft coral, although canventol has a simpler structure than sarcophytol A. Their mechanisms of action were studied based on our recent evidence that tumor necrosis factor release induced by okadaic acid is an essential mechanism of tumor promotion. Canventol inhibited mouse tumor necrosis factor release from BALB/3T3 cells less strongly than sarcophytol A, indicating that canventol has additional activity. Canventol inhibited isoprenylation of proteins with various molecular weights, such as M_r 22,000, 17,000, and 13,000, whereas sarcophytol A did not show significant inhibition. Thus, a potent anticarcinogenic activity of canventol is mediated through the inhibitory bifunctions of tumor necrosis factor release and of protein isoprenylation. Since canventol is less toxic to cells than sarcophytol A, these bifunctions are useful markers for screening for new cancer chemopreventive agents.

¹ This work was supported in part by Grants-in-Aid for Cancer Research from the Ministry of Education, Science and Culture, a grant from the Ministry of Health and Welfare for a Comprehensive 10-Year Strategy for Cancer Control, Japan, and grants from the Foundation for Promotion of Cancer Research, the Uehara Memorial Life Science Foundation, the Princess Takamatsu Cancer Research Fund, and the Smoking Research Foundation.

² To whom requests for reprints should be addressed.

Received 4/29/93. Accepted 6/17/93.

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