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Titolo:
Neither fibroblast growth factor-1 nor fibroblast growth factor-2 is an androgen receptor coactivator in androgen-resistant prostate cancer
Autore:
Shain, SA;
Indirizzi:
Univ Texas, Hlth Sci Ctr San Antonio, Dept Obstet & Gynecol, San Antonio, TX 78229 USA Univ Texas San Antonio TX USA 78229 & Gynecol, San Antonio, TX 78229 USA
Titolo Testata:
MOLECULAR UROLOGY
fascicolo: 3, volume: 5, anno: 2001,
pagine: 121 - 130
SICI:
1091-5362(200123)5:3<121:NFGFNF>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
SIGNAL-TRANSDUCTION PATHWAYS; ESTROGEN-RECEPTOR; CARCINOMA-CELLS; FACTOR-I; TRANSCRIPTIONAL COACTIVATOR; TRANSACTIVATION DOMAIN; PHOSPHORYLATION SITES; INDEPENDENT PATHWAYS; HISTONE DEACETYLASE; HORMONE-BINDING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
67
Recensione:
Indirizzi per estratti:
Indirizzo: Shain, SA Univ Texas, Hlth Sci Ctr San Antonio, Dept Obstet & Gynecol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA Univ Texas 7703 Floyd Curl Dr San Antonio TX USA 78229 78229 USA
Citazione:
S.A. Shain, "Neither fibroblast growth factor-1 nor fibroblast growth factor-2 is an androgen receptor coactivator in androgen-resistant prostate cancer", MOL UROL, 5(3), 2001, pp. 121-130

Abstract

We used rat prostate cancer cell stable transfectants that lacked either endogenous fibroblast growth factor (FGF)-1 secondary to constitutive expression of FGF-1 antisense RNA (aFa2-transfeetants) or endogenous FGF-2 isoforms secondary to constitutive expression of FGF-2 antisense RNA (bFa9-transfectants) to examine the potential synergistic effects of mitogen and androgen as modulators of proliferation. During culture on 5% charcoal-stripped fetal bovine serum (CS-FBS), FGF-1 caused a 2- to 2.5-fold increase in the proliferation of aFa2-transfectants that lacked endogenous FGF-1 and retained full expression of FGF-2 isoforms. In marked constrast, bFa9-transfectants that lacked FGF-2 isoforms and retained full expression of FGF-1 died with exponential kinetics when cultured on either 5% CS-FBS or 5% FBS in the absence of FGF-2. However, FGF-2 promoted bFa9-transfectant survival and exponential proliferation during culture on either 5% CS-FBS or 5% FBS. The nonmetabolizable androgen R1881 did not affect proliferation of either the aFa2-transfectants, the bFa9-transfectants, or the parental prostate cancer cells used to generate these transfectants. Additionally, neither of the androgen receptor antagonists RU23908 or bicalutamide affected either FGF-1-mediated aFa2-transfectant proliferation or FGF-2-mediated bFa9-transfectant proliferation during culture on 5% CS-FBS. Notably, transient transfection analyses established R1881 concentration-dependent induction of chloramphenicol acetyltransferase activity in both aFa2-transfectants and bFa9-transfectants. Thus, the failure of either androgen or antiandrogen to affect either FGF-mediated or FGF-independent antisense-transfectant proliferation is not attributable to absence of functional androgen receptors. The results indicate that FGF effects in these androgen-resistant antisense transfectants do not involve either androgen-dependent or androgen-independent, mitogen-mediated androgen receptor activation. Our studies show that these rat prostate cancer cells are characterized by both retention of functional androgen receptors during development of androgen resistance and mitogen-mediated, autocrine or paracrine (or both) modulated proliferation. These are two prominent properties characteristic of advanced human prostate cancer.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/01/21 alle ore 03:24:07