Tumor promoters enhance cap formation in mouse thymocytes

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Abstract
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, 4α-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 Ca 2+ -dependent process involving the submembrane actin filaments.