Changes in the 32P incorporation in rat mammary tumor after chronic administration of LH-RH analogs.
We studied endogenous phosphorylation in rat transplantable MT/W9A hormone-dependent mammary tumors of untreated rats and of animals treated with LH-RH analogs, the agonist D-Trp-6-LH-RH and the antagonist N-Ac-D-p-Cl-Phe1,2,D-Trp3,D-Arg6,D-Ala10-LH-RH. Incorporation of 32P from 32P-ATP was reduced significantly in tumors of rats treated with agonistic and antagonistic analogs of LH-RH or ovariectomized. The inhibition of protein phosphorylation may be related to tumor regression.
D000818:Animals; D001345:Autoradiography; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives* / Q000494:pharmacology; D008325:Mammary Neoplasms, Experimental / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000378:metabolism*; D009376:Neoplasms, Hormone-Dependent / Q000378:metabolism; D010052:Ovariectomy; D010761:Phosphorus Radioisotopes; D010766:Phosphorylation; D051381:Rats; D011920:Rats, Inbred WF; D017329:Triptorelin Pamoate
D009363:Neoplasm Proteins; D010761:Phosphorus Radioisotopes; D017329:Triptorelin Pamoate; D007987:Gonadotropin-Releasing Hormone; C042691:LHRH, N-acetyl-(4-chlorophenylalanyl)(1)-(4-chlorophenylalanyl)(2)-tryptophyl(3)-arginyl(6)-alanine(10)-