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• W2078657475 endingPage "13" @default.
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• W2078657475 abstract "Although ovaries serve as the primary source of estrogen for pre-menopausal women, after menopause estrogen biosynthesis from circulating precursors occurs in peripheral tissues by the action of several enzymes, 17β-hydroxysteroid dehydrogenase 1 (17β-HSD1), aromatase and estrogen sulfatase. In the breast, both normal and tumoral tissues have been shown to be capable of synthesizing estrogens, and this local estrogen production can be implicated in the development of breast tumors. In these tissues, estradiol (E2) can be synthesized by three pathways: (1) estrone sulfatase transforms estrogen sulfates into bioactive estrogens, (2) 17β-HSD1 converts estrone (E1) into E2, (3) aromatase which converts androgens into estrogens is also present and contributes to the in situ synthesis of active estrogens but to a far lesser extent than estrone sulfatase. Quantitative assessment of E2 formation in human breast tumors indicates that metabolism of estrone sulfate (E1S) via the sulfatase pathway produces 100–500 times more E2 than androgen aromatization. Breast tissue also possesses the estrogen sulfotransferase involved in the conversion of estrogens into their sulfates that are biologically inactive. In the present review, we summarized the action of the 19-nor-progestin nomegestrol acetate (NOMAC) on the sulfatase, 17β-HSD1 and sulfotransferase activities in the hormone-dependent MCF-7 and T47-D human breast cancer cell lines. Using physiological doses of substrates NOMAC blocks very significantly the conversion of E1S to E2. It inhibits the transformation of E1 to E2. NOMAC has a stimulatory effect on sulfotransferase activity in both cell lines, with a strong stimulating effect at low doses but only a weak effect at high concentrations. The effects on the three enzymes are always stronger in the progesterone-receptor rich T47-D cell line as compared with the MCF-7 cell line. Besides, no effect is found for NOMAC on the transformation of androstenedione to E1 in the aromatase-rich choriocarcinoma cell line JEG-3. In conclusion, the inhibitory effect provoked by NOMAC on the enzymes involved in the biosynthesis of E2 (sulfatase and 17HSD pathways) in estrogen-dependent breast cancer, as well as the stimulatory effect on the formation of the inactive E1S, can open attractive perspectives for future clinical trials." @default.
• W2078657475 created "2016-06-24" @default.
• W2078657475 creator A5002437874 @default.
• W2078657475 creator A5009706537 @default.
• W2078657475 creator A5014461731 @default.
• W2078657475 creator A5038373321 @default.
• W2078657475 date "2005-01-01" @default.
• W2078657475 modified "2023-10-04" @default.
• W2078657475 title "Effect of nomegestrol acetate on estrogen biosynthesis and transformation in MCF-7 and T47-D breast cancer cells" @default.
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