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Titolo:
Novel antitumor effect of estradiol in athymic mice injected with a T47D breast cancer cell line overexpressing protein kinase C alpha
Autore:
Chisamore, MJ; Ahmed, Y; Bentrem, DJ; Jordan, VC; Tonetti, DA;
Indirizzi:
Northwestern Univ, Sch Med, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA Northwestern Univ Chicago IL USA 60611 ns Canc Ctr, Chicago, IL 60611 USA Northwestern Univ, Sch Med, Dept Surg, Chicago, IL 60611 USA Northwestern Univ Chicago IL USA 60611 , Dept Surg, Chicago, IL 60611 USA
Titolo Testata:
CLINICAL CANCER RESEARCH
fascicolo: 10, volume: 7, anno: 2001,
pagine: 3156 - 3165
SICI:
1078-0432(200110)7:10<3156:NAEOEI>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
ESTROGEN-RECEPTOR-BETA; TRANSCRIPTIONAL ACTIVATION; RESPONSE ELEMENT; AP-1 ACTIVITY; TAMOXIFEN; TUMORS; EXPRESSION; ANTIESTROGENS; PHENOTYPE; DIETHYLSTILBESTROL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Tonetti, DA Univ Illinois, Coll Pharm, Dept Pharmaceut & Pharmacodynam MC865, 833 S Wood St, Chicago, IL 60612 USA Univ Illinois 833 S Wood St Chicago IL USA 60612 IL 60612 USA
Citazione:
M.J. Chisamore et al., "Novel antitumor effect of estradiol in athymic mice injected with a T47D breast cancer cell line overexpressing protein kinase C alpha", CLIN CANC R, 7(10), 2001, pp. 3156-3165

Abstract

Purpose: Resistance to tamoxifen (TAM) represents a significant challenge to the management of breast cancer. We previously reported that the estrogen receptor (ER)negative hormone-independent T47D:C42 cell line has both elevated protein kinase C alpha (PKC alpha) protein expression and basal activator protein-1 activity compared with the parental ER+ (hormone-dependent) T47D:A18 cell line. Stable transfection of PKC alpha to the T47D:A18 breastcancer cell line results in increased basal activator protein-1 activity, reduced ER function, increased proliferation rate, and hormone-independent growth (Tonetti et al., Br. J. Cancer, 83: 782-791, 2000). In this report, we further characterize the role of PKC alpha overexpression in vivo to elucidate a possible molecular mechanism of tamoxifen resistance. Experimental Design: To determine whether the T47D: A18/PKC alpha cell line would produce hormone-independent tumors in athymic mice, we injected T47D:A18, T47D:A18/neo, or the T47D:A18/PKC alpha 20 cell clones bilaterally into the mammary fat pads of athymic mice. Tumor growth was evaluated following treatment with estradiol (E2), TAM, and the pure antiestrogen, ICI 182,780. Results: Mice receiving either T47D:A18 or T47D:A18/neo cells produced tumors that grew in response to E2 treatment, whereas the untreated control and TAM-treated groups showed no tumor growth. Interestingly, mice receiving the T47D:A18/PKC alpha 20 clone produced tumors in both the control and TAMgroups, whereas tumor growth was inhibited in mice treated with E2. PKC alpha was also overexpressed in an MCF-7 tumor model that also exhibited TAM-stimulated and E2-induced regression. Conclusions: These results suggest that overexpression of PKC alpha in breast tumors results in hormone-independent tumor growth that cannot be inhibited by TAM treatment. Furthermore, the finding that E2 has an antitumor effect on breast tumors overexpressing PKC alpha is a novel observation that may have important therapeutic implications.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/21 alle ore 02:31:37