Differential effects of tumor promoters on cAMP production: inhibition of receptor-mediated and potentiation of cholera toxin-mediated stimulation.
Tetradecanoylphorbol-acetate and other tumor promoters inhibit prostaglandin E2 and isoproterenol-induced cAMP accumulation in mouse thymocytes but markedly potentiate cAMP production induced by cholera toxin. Cholera toxin is known to stimulate cAMP production by inducing ADP-ribosylation of the alpha-subunit of a guanine nucleotide-binding regulatory (G) protein, resulting in activation of the catalytic unit of adenylate cyclase. G proteins have been implicated as plasma membrane transducers for a variety of additional signals. It is possible that the growth promoting and co-mitogenic properties of tumor promoters are related to their effects on G proteins.
D000818:Animals; D002273:Carcinogens / Q000494:pharmacology*; D002772:Cholera Toxin / Q000494:pharmacology*; D000242:Cyclic AMP / Q000096:biosynthesis*; D015232:Dinoprostone; D004357:Drug Synergism; D019204:GTP-Binding Proteins / Q000378:metabolism*; D066298:In Vitro Techniques; D007700:Kinetics; D051379:Mice; D008807:Mice, Inbred BALB C; D011458:Prostaglandins E / Q000494:pharmacology; D011975:Receptors, Mitogen / Q000032:analysis; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013950:Thymus Gland / Q000187:drug effects
D002273:Carcinogens; D011458:Prostaglandins E; D011975:Receptors, Mitogen; C038223:peanut agglutinin receptor; D002772:Cholera Toxin; D000242:Cyclic AMP; D019204:GTP-Binding Proteins; D015232:Dinoprostone; D013755:Tetradecanoylphorbol Acetate