Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Estradiol inhibits glucocorticoid receptor expression and induces glucocorticoid resistance in MCF-7 human breast cancer cells
Autore:
Krishnan, AV; Swami, S; Feldman, D;
Indirizzi:
Stanford Univ, Sch Med, Dept Med, Div Endocrinol, Stanford, CA 95305 USA Stanford Univ Stanford CA USA 95305 iv Endocrinol, Stanford, CA 95305 USA
Titolo Testata:
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
fascicolo: 1, volume: 77, anno: 2001,
pagine: 29 - 37
SICI:
0960-0760(200104)77:1<29:EIGREA>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
GENE-EXPRESSION; ESTROGEN-RECEPTOR; POSTMENOPAUSAL WOMEN; GROWTH; PREDNISOLONE; CULTURE; CYCLE; RAT; QUANTITATION; PROGESTERONE;
Keywords:
estrogen; glucocorticoid receptor; glucocorticoid action; breast cancer; MCF-7;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Feldman, D Stanford Univ, Sch Med, Dept Med, Div Endocrinol, 300 Pasteur Dr, Stanford, CA 95305 USA Stanford Univ 300 Pasteur Dr Stanford CA USA 95305 CA 95305 USA
Citazione:
A.V. Krishnan et al., "Estradiol inhibits glucocorticoid receptor expression and induces glucocorticoid resistance in MCF-7 human breast cancer cells", J STEROID B, 77(1), 2001, pp. 29-37

Abstract

Our study has shown that treatment of MCF-7 human breast cancer cells with17-beta estradiol (E-2) produced significant decreases in glucocorticoid receptor (GR) concentrations and CR mRNA levels. E-2 pre-treatment of MCF-7 cells stably transfected with the GR responsive pMTV-CAT reporter (MCF-7 MTV cells), caused significant attenuation of dexamethasone (DEX)-induced chloramphenicol acety] transferase (CAT). In MCF-7 cells transiently transfected with [(GRE)(3)-Luc] reporter plasmid. E-2 pre-treatment significantly suppressed DEX-induced luciferase, which was abolished by the estrogen receptor antagonist ICI 182,780. We examined the effect of chronic E-2 treatment as well as E-2 withdrawal on GR Function and abundance. MCF-7-MTV cells were treated with vehicle (control) or E-2 for up to 16 days. A third group received E-2 for 5 days followed by E-2 withdrawal from day 6 to 16. Chronic E-2 treatment almost totally abrogated DEX-induced CAT and reduced GR to very low levels. Interestingly, in the group subjected to E-2 withdrawal, neither the DEX response nor GR abundance recovered and reached control valuessuggesting that the estrogen mediated suppression is long lasting and could not be easily reversed. The E-2 induced resistance to glucocorticoid action may be of potential clinical significance in a number of settings including breast cancer, neuroendocrine response to stress and osteoporosis and could possibly contribute to the differences in glucocorticoid responsiveness among patients. (C) 2001 Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 09:26:18