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© 1983 Oxford University Press

research-article

Tumor promoters enhance cap formation in mouse thymocytes

C. Cherif-Zahar 1, P. Vaigot 2 and M. Castagna 1 3

1Institut de Recherches Scientifiques sur le Cancer 7 rue Guy Mocquet, B.P. 8, 94802 Villejuif Cedex
2Institut de Cancerologie et d'Immunogénétique 14 Avenue P.V. Couturier, 94800 Villejuif Cedex, France

3To whom all correspondence should be sent

Potent tumor promoters such as 12-O-tetradecanoylphorbol 13-acetate (TPA) and teleocidin, rapidly evoked a dose-dependent stimulation of concanavalin A (Con A)-nduced cap formation in mouse T lymphocytes. The effect was reversible upon removal of the drugs. Weaker tumor promoters, phorbol didecanoate, phorbol dibenzoate and iodoacetic acid stimulated capping to a lower extent. Mezerein, a phorbol-related macrocyclic diterpene derivative, which acts as a second-stage promoter was also active in increasing the number of caps. In contrast, 4{alpha}-phorbol didecanoate and phorbol which are devoid of tumor promoting activity, did not affect capping. Anti-promoting glucocorticoids inhibited capping stimulation. Flow cytofluorometric analysis of Con A binding has shown that TPA did not modify the lectin binding to surface receptors. TPA-fadlitated capping was energy-dependent. Cytochalasin B prevented the TPA-induced response whereas colchicine was ineffective. Phenothiazines fully inhibited the TPA effect, thus suggesting that tumor-promoter-mediated lectin receptor redistribution may be ascribed to the facilitation of a Ca2+-dependent process involving the submembrane actin filaments.


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