During the growth arrest of 7,12-dimethylbenz(alpha)
anthracene-induced rat mammary
carcinomas following
ovariectomy or N6, O2'-dibutyryl cyclic
adenosine 3':5'-monophosphate (
DBcAMP) treatment, a change in the specific
estrogen and cAMP binding to
tumor proteins is observed. Three days after
ovariectomy or
DBcAMP treatment of the hosts, cAMP binding increases 5- and 2-fold in the nuclei and cytosol of
tumors, respectively, whereas nuclear and cytoplasmic
estrogen binding decreases by 70 and 25%, respectively. These changes in cAMP- and
estrogen-binding activities are detectable within 1 day after
ovariectomy or
DBcAMP treatment, and the changes are reversed when resumption of
tumor growth is induced by the injection of
estradiol valerate or cessation of
DBcAMP treatment. When 7,12-dimethylbenz(alpha)anthracene-induced
tumors fail to regress after
ovariectomy or
DBcAMP treatment, the change in
estrogen and cAMP binding does not occur. Concomitant with the increase of cAMP-binding activity in regressing
tumors are increases in
histone kinase activity and the cAMP content of the
tumors. These increases in cAMP-binding and
protein kinase activities are blocked by
cycloheximide. These data suggest an interaction between a
steroid hormone and cAMP in the growth control of a
hormone-dependent mammary
tumor.