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Titolo:
Estrogen mitogenic action. II. Negative regulation of the steroid hormone-responsive growth of cell lines derived from human and rodent target tissuetumors and conceptual implications
Autore:
Sirbasku, DA; Moreno-Cuevas, JE;
Indirizzi:
Univ Texas, Hlth Sci Ctr, Houston, TX 77225 USA Univ Texas Houston TX USA77225 exas, Hlth Sci Ctr, Houston, TX 77225 USA
Titolo Testata:
IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL
fascicolo: 7, volume: 36, anno: 2000,
pagine: 428 - 446
SICI:
1071-2690(200007/08)36:7<428:EMAINR>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN-BREAST-CANCER; HUMAN-PROSTATE-CANCER; CHEMICALLY-DEFINED MEDIUM; SERUM-FREE CULTURE; FACTOR-BETA; FACTOR-ALPHA; RECEPTOR SUPERFAMILY; EPITHELIAL-CELLS; MESSENGER-RNA; KIDNEY TUMOR;
Keywords:
human breast cancer; human prostate cancer; rat pituitary tumors; hamster kidney tumors; serum inhibitor; estrogens; androgens; progesterone; cortisol; epidermal growth factor; transforming growth factor alpha; transforming growth factor beta; insulin-like growth factors;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
165
Recensione:
Indirizzi per estratti:
Indirizzo: Sirbasku, DA Univ Texas, Sch Med, Dept Biochem & Mol Biol, 6431 Fannin St,Houston, TX 77030 USA Univ Texas 6431 Fannin St Houston TX USA 77030 , TX 77030 USA
Citazione:
D.A. Sirbasku e J.E. Moreno-Cuevas, "Estrogen mitogenic action. II. Negative regulation of the steroid hormone-responsive growth of cell lines derived from human and rodent target tissuetumors and conceptual implications", IN VITRO-AN, 36(7), 2000, pp. 428-446

Abstract

In an accompanying report (Moreno-Cuevas, J. E.; Sirbasku, D. A., In VitroCell. Dev. Biol.; 2000), we demonstrated 80-fold estrogen mitogenic effects with MTW9/PL2 rat mammary tumor cells in cultures supplemented with charcoal-dextran-treated serum. All sera tested contained an estrogen reversibleinhibitor(s). The purpose of this report is to extend those observations to additional sex steroid-responsive human and rodent cell lines. Every linetested showed a biphasic response to hormone-depleted serum. Concentrations of less than or equal to 10% (v/v) promoted substantive growth. At higherconcentrations, serum was progressively inhibitory. With estrogen receptor-positive (ER+) human breast cancer cells, rat pituitary tumor cells, and Syrian hamster kidney tumor cells, 50% (v/v) serum caused significant inhibition, which was reversed by very low physiologic concentrations of estrogens. This same pattern was observed with the steroid hormone-responsive LNCaPhuman prostatic carcinoma cells. Because steroid hormone mitogenic effectsare now easily demonstrable using our new methods, the identification of positive results has nullified our original endocrine estromedin hypothesis. We also evaluated autocrine/paracrine growth factor models of estrogen-responsive growth. We asked if insulin-like growth factors I and II, insulin, transforming growth factor alpha, or epidermal growth factor substituted for the positive effects of estrogens. Growth factors did not reverse the serum-caused inhibition. We asked also if transforming growth factor beta (TGFbeta) substituted for the serum-borne inhibitor. TGF beta did not substitute. Altogether, our results are most consistent with the concept of a unique serum-borne inhibitor as has been proposed in the estrocolyone model. However, the aspect of the estrocolyone model related to steroid hormone mechanism of action requires more evaluation. The effects of sex steroids at picomolar concentrations may reflect mediation via inhibitor "activated" intracellular signaling pathways.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 01:38:08