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Titolo:
Effect of long-term estrogen deprivation on apoptotic responses of breast cancer cells to 17 beta-estradiol
Autore:
Song, RXD; Mor, G; Naftolin, F; McPherson, RA; Song, J; Zhang, ZG; Yue, W; Wang, JP; Santen, RJ;
Indirizzi:
Univ Virginia, Hlth Sci Ctr, Div Endocrinol, Sch Med,Dept Internal Med, Charlottesville, VA 22908 USA Univ Virginia Charlottesville VA USA 22908 Charlottesville, VA 22908 USA Yale Univ, Sch Med, Dept Obstet & Gynecol, New Haven, CT 06510 USA Yale Univ New Haven CT USA 06510 bstet & Gynecol, New Haven, CT 06510 USA
Titolo Testata:
JOURNAL OF THE NATIONAL CANCER INSTITUTE
fascicolo: 22, volume: 93, anno: 2001,
pagine: 1714 - 1723
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATION-INDUCED APOPTOSIS; FAS/FAS-LIGAND SYSTEM; MYC-INDUCED APOPTOSIS; FAS-LIGAND; ESTRADIOL HYPERSENSITIVITY; RANDOMIZED TRIAL; MAP KINASE; IN-VIVO; C-MYC; TAMOXIFEN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Santen, RJ Univ Virginia, Hlth Sci Ctr, Div Endocrinol, Sch Med,Dept Internal Med, Charlottesville, VA 22908 USA Univ Virginia Charlottesville VA USA 22908 ville, VA 22908 USA
Citazione:
R.X.D. Song et al., "Effect of long-term estrogen deprivation on apoptotic responses of breast cancer cells to 17 beta-estradiol", J NAT CANC, 93(22), 2001, pp. 1714-1723

Abstract

Background: High doses of estrogen can promote tumor regression in postmenopausal women with hormone-dependent breast cancer, but the mechanism is unknown. We investigated the molecular basis of this process by using LTED cells, which were derived by growing MCF-7 breast cancer cells under long-term (6-24 months) estrogen-deprived conditions. Methods: We treated LTED and MCF-7 cells with various concentrations of 17 beta -estradiol (estradiol) and assayed their growth by counting the cells and measured apoptosis by annexin V staining and DNA fragmentation. Using western blot analysis, we alsoexamined the expression of the apoptosis-inducing system of the Fas death receptor protein and its ligand, FasL, in these cells. To assess the involvement of Fas and FasL in the induction of apoptosis in LTED cells, we used activating anti-Fas antibodies and the universal caspase inhibitor Z-VAD. Finally, we examined the expression of Fas protein in E8CASS and BSK3 cells,two other cell lines derived by depriving MCF-7 cells of estrogen long term, and the responses of these cells to high-dose estradiol: All statisticaltests were two-sided. Results: High concentrations of estradiol (greater than or equal to0.1 nM) resulted in a statistically significant, 60% reduction in the growth of LTED cells (P < .001) and in a sevenfold increase in apoptosis (P < .001) as compared with levels in vehicle-treated cells. Both LTED and MCF-7 cells expressed FasL, but only LTED cells expressed Fas. Treatment of LTED cells with 0.1 nM estradiol increased the expression of FasL. Activating anti-Fas antibodies increased apoptosis of LTED cells, which was further stimulated by estradiol. Z-VAD blocked estradiol-induced apoptosis. E8CASS cells, which express Fas protein, but not BSK3 cells, which do not, also responded to 0.1 nM estradiol by increasing apoptosis. Conclusion: Tumor regression induced by high-dose estrogen therapy in postmenopausal woman may result from estrogen activation of Fas-mediated apoptosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 08/04/20 alle ore 10:49:51