title: Inhibition by Celiptium of the fetal thymidine kinase synthesis induced by estrogens in the rat uterus.
abstract: Celiptium (Ce) is an antitumor drug used in the therapy of breast carcinomas, which are to a large extent dependent on estrogens. We have studied the effect of Ce on some proteins induced by estradiol (E2) in the rat uterus. It was observed that Ce administered at the same time or before E2, was able to inhibit the induction by E2 of fetal thymidine kinase (TK-F), of creatine kinase of brain-type (CK-BB) and of progesterone receptor (PR). When Ce was given after E2, its inhibitory effects were less evident. Results seemed to indicate that Ce could bind the acceptor sites for E2 receptor and thus inhibit the activity of E2-regulated genes. This assumption was corroborated by the fact that Ce did not modify the activity of enzymes not submitted to E2 regulation.
mesh_terms: D000470:Alkaloids / Q000494:pharmacology*; D000818:Animals; D003402:Creatine Kinase / Q000378:metabolism; D004611:Ellipticines / Q000494:pharmacology*; D004958:Estradiol / Q000494:pharmacology; D004965:Estrogen Antagonists; D005260:Female; D007527:Isoenzymes / Q000378:metabolism; D010735:Phosphoglycerate Kinase / Q000378:metabolism; D011770:Pyruvate Kinase / Q000378:metabolism; D051381:Rats; D011980:Receptors, Progesterone / Q000378:metabolism; D013937:Thymidine Kinase / Q000096:biosynthesis / Q000378:metabolism*; D014599:Uterus / Q000201:enzymology*
chemical_list: D000470:Alkaloids; D004611:Ellipticines; D004965:Estrogen Antagonists; D007527:Isoenzymes; D011980:Receptors, Progesterone; C027767:elliptinium; D004958:Estradiol; D013937:Thymidine Kinase; D011770:Pyruvate Kinase; D010735:Phosphoglycerate Kinase; D003402:Creatine Kinase