Tumour promoter uncouples β-adrenergic receptor from adenyl cyclase in mouse epidermis

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Abstract
Alterations in β-adrenergic receptor number and function and in the hormonal responsiveness of adenylate cyclase have been observed in transformed cells1–3, and tumours4,5. Phorbol myristate acetate (PMA), a potent tumour promoter in mouse skin, induces a dramatic loss of epidermal responsiveness to catecholamines in vivo6,8, although basal levels of cyclic AMP are not affected7–9. In other work we have shown that PMA treatment does not alter the number or affinity of epidermal β-receptors, although accumulation of cyclic AMP in response to isoprenaline injection is sharply inhibited10. Evidence is presented here that PMA exerts this effect by uncoupling epidermal β-receptors from adenylate cyclase.