Hypothesis. Cyclic AMP and its receptor protein in tumor growth regulation in vivo.
A working hypothesis is presented to elucidate the action of cyclic AMP in the regulation of tumor growth in vivo. The formation and nuclear translocation of a complex consisting of cyclic AMP, its receptor binding protein, and the catalytic unit of protein kinase are the indispensable events necessary to trigger the regression of hormone-dependent mammary tumors. If the integrity of the cyclic AMP receptor molecule is not preserved and the cyclic AMP concentration is not physiological, the above processes do not occur and tumors remain hormone-unresponsive. It is therefore postulated that arrest of tumor growth in vivo depends upon the structural integrity of the cyclic AMP receptor protein and the optimum cellular concentration of cyclic AMP, which make possible the formation and nuclear translocation of the cyclic AMP receptor complex.
D000818:Animals; D002369:Castration; D002467:Cell Nucleus / Q000378:metabolism; D055598:Chemical Phenomena; D002621:Chemistry; D000242:Cyclic AMP / Q000378:metabolism*; D003600:Cytosol / Q000378:metabolism; D005260:Female; D008325:Mammary Neoplasms, Experimental / Q000378:metabolism* / Q000503:physiopathology; D008954:Models, Biological; D010766:Phosphorylation; D011494:Protein Kinases / Q000378:metabolism; D051381:Rats; D011953:Receptors, Cyclic AMP / Q000378:metabolism*
D011953:Receptors, Cyclic AMP; D000242:Cyclic AMP; D011494:Protein Kinases