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Comparative Effects of Aplysiatoxin, Debromoaplysiatoxin, and Teleocidin on Receptor Binding and Phospholipid Metabolism¹

Division of Environmental Science and Cancer Center/Institute of Cancer Research, Columbia University, College of Physicians and Surgeons, New York, New York, 10032 [A. D. H., I. B. W., A. J., E. O.]; National Cancer Center Research Institute, Tsukiji 5-1-1, Chuo-Ku, Tokyo 104, Japan [H. F., T. S.]; and Department of Chemistry, University of Hawaii, Honolulu, Hawaii 96822 [R. E. M.]

We have compared the activities of aplysiatoxin and debromoaplysiatoxin, two polyacetate marine algae toxins, with teleocidin, a tumor-promoting indole alkaloid from Streptomyces, with respect to inhibition of specific binding of epidermal growth factor, and phorbol-12,13-dibutyrate to their respective receptors and ability to stimulate the release of radioactivity from cells prelabeled with choline or arachidonic acid. Although these compounds have chemical structures that are quite different from the phorbol esters, both aplysiatoxin and teleocidin are essentially equipotent with the potent tumor promoter 12-O-tetradecanoylphorbol-13-acetate in all four assays. The fact that aplysiatoxin and teleocidin inhibit phorbol-12,13-dibutyrate-receptor binding suggests that their biological activities are mediated by binding to the same receptors utilized by the phorbol esters. Debromoaplysiatoxin, a debrominated form of aplysiatoxin, is about 10-fold weaker than aplysiatoxin in inhibiting epidermal growth factor and phorbol-12,13-dibutyrate-receptor binding, but is equipotent with aplysiatoxin in stimulating the release of lipid metabolites from the prelabeled cells. The results are discussed in terms of possible heterogeneity of cellular receptors for this group of compounds.

¹ This work was supported in part by Grants-in-aid for Cancer Research from the Ministry of Education, Science and Culture of Japan, the Princess Takamatsu Cancer Research Fund, the United States-Japan Cooperative Cancer Research Program, and a research fellowship from the DuPont Company.

² Recipient of National Cancer Institute Grant CA 26056. To whom requests for reprints should be addressed.

³ Recipient of National Cancer Institute Grant CA 12632.

Received 6/ 9/82. Accepted 12/10/82.

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