Tumor promoters enhance cap formation in mouse thymocytes.
Potent tumor promoters such as 12-O-tetradecanoylphorbol 13-acetate (TPA) and teleocidin, rapidly evoked a dose-dependent stimulation of concanavalin A (Con A)-induced 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-facilitated 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.
D000818:Animals; D002273:Carcinogens / Q000494:pharmacology*; D002465:Cell Movement / Q000187:drug effects; D007152:Immunologic Capping / Q000187:drug effects*; D066298:In Vitro Techniques; D037102:Lectins / Q000494:pharmacology; D051379:Mice; D010640:Phenothiazines / Q000494:pharmacology; D010704:Phorbols / Q000494:pharmacology*; D013601:T-Lymphocytes / Q000187:drug effects / Q000648:ultrastructure*; D013696:Temperature; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*; D013997:Time Factors
D002273:Carcinogens; D037102:Lectins; D010640:Phenothiazines; D010704:Phorbols; D013755:Tetradecanoylphorbol Acetate