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Cyclic AMP-binding proteins: inverse relationship with estrogen-receptors in hormone-dependent mammary tumor

Y S Cho-Chung, J S Bodwin, T Clair

    European Journal of Biochemistry
    |May 1, 1978
    PubMed

    Insights

    Ovariectomy-induced regression of dimethylbenzanthracene (DBA)-induced rat mammary tumors alters cyclic adenosine 3':5'-monophosphate (cAMP) and estrogen binding. These changes indicate cAMP

    Area of Science:

    • Endocrinology
    • Molecular Biology
    • Oncology

    Background:

    • Dimethylbenzanthracene (DBA)-induced rat mammary tumors exhibit binding activities for cyclic adenosine 3 :5 '-monophosphate (cAMP) and estrogen.
    • Hormonal regulation, particularly estrogen, plays a role in the growth of these hormone-dependent tumors.

    Purpose of the Study:

    • To investigate the changes in cAMP and estrogen binding activities in DBA-induced rat mammary tumors following ovariectomy.
    • To explore the role of cAMP in the growth control of hormone-dependent mammary tumors.

    Main Methods:

    • Induction of rat mammary tumors using dimethylbenzanthracene.
    • Ovariectomy of tumor-bearing rats to induce tumor regression.
    • Measurement of cAMP and estrogen binding activities in tumor nuclei and cytosol.
    • Assay of adenylate cyclase, cAMP-phosphodiesterase, and histone kinase activities.
    • Hormonal manipulation using 17beta-estradiol to reverse tumor growth.

    Main Results:

    • Ovariectomy led to tumor regression and significant alterations in cAMP and estrogen binding.
    • cAMP binding increased 5-fold in nuclei and 2-fold in cytosol, while estrogen binding decreased by 80% (nuclear) and 50% (cytoplasmic) within 6 days post-ovariectomy.
    • These changes were detectable within 1 day and reversible with 17beta-estradiol administration.
    • Regressing tumors showed increased cAMP levels, adenylate cyclase, cAMP-phosphodiesterase, and histone kinase activities.

    Conclusions:

    • The observed changes in cAMP and estrogen binding activities are strongly associated with the regression of hormone-dependent mammary tumors.
    • Increased cAMP levels and associated enzyme activities in regressing tumors suggest a significant role for cAMP in the growth control of these tumors.
    • These findings highlight the complex interplay between hormonal influences and intracellular signaling pathways in mammary tumor progression and regression.

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