Dibutyryl cyclic AMP mimics ovariectomy: nuclear protein phosphorylation in mammary tumor regression

Growth of mammary carcinoma induced by 7,12-dimethyl-benz(a) anthracene is arrested by either ovariectomy or treatment with N6,O2-dibutyryl cyclic adenosine 3',5'-monophosphate (dibutyryl cyclic AMP). When this occurs, a new nonhistone protein species becomes the predominant endogenous substrate of cyclic AMP-dependent protein kinase in the tumor nuclei. Phosphorylation of this regression-associated protein ceases when resumption of tumor growth is induced by either the injection of 17 beta-estradiol or cessation of dibutyryl cyclic AMP treatment. Thus phosphorylation of regression-associated protein may play a role in the regression of hormone-dependent mammary tumors.