Glycitein activates extracellular signal-regulated kinase via vascular endothelial growth factor receptor signaling in nontumorigenic (RWPE-1) prostate epithelial cells.
J Nutr Biochem
; 18(8): 525-32, 2007 Aug.
Article
em En
| MEDLINE
| ID: mdl-17156992
ABSTRACT
Increased consumption of soy is associated with a decreased risk for prostate cancer; however, the specific cellular mechanisms responsible for this anticancer activity are unknown. Dietary modulation of signaling cascades controlling cellular growth, proliferation and differentiation has emerged as a potential chemopreventive mechanism. The present study examined the effects of four soy isoflavones (genistein, daidzein, glycitein and equol) on extracellularsignal-regulated kinase (ERK1/2) activity in a nontumorigenic prostate epithelial cell line (RWPE-1). All four isoflavones (10 micromol/L) significantly increased ERK1/2 activity in RWPE-1 cells, as determined by immunoblotting. Isoflavone-induced ERK1/2 activation was rapid and sustained for approximately 2 h posttreatment. Glycitein, the most potent activator of ERK1/2, decreased RWPE-1 cell proliferation by 40% (P<.01). Glycitein-induced ERK1/2 activation was dependent, in part, on tyrosine kinase activity associated with vascular endothelial growth factor receptor (VEGFR). The presence of both VEGFR1 and VEGFR2 in the RWPE-1 cell line was confirmed by immunocytochemistry. Treatment of RWPE-1 cells with VEGF(165) resulted in transient ERK1/2 activation and increased cellular proliferation. The ability of isoflavones to modulate ERK1/2 signaling cascade via VEGFR signaling in the prostate may be responsible, in part, for the anticancer activity of soy.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Próstata
/
Receptores de Fatores de Crescimento do Endotélio Vascular
/
Proteína Quinase 3 Ativada por Mitógeno
/
Fitoestrógenos
/
Células Epiteliais
/
Isoflavonas
Limite:
Humans
/
Male
Idioma:
En
Revista:
J Nutr Biochem
Assunto da revista:
BIOQUIMICA
/
CIENCIAS DA NUTRICAO
Ano de publicação:
2007
Tipo de documento:
Article
País de afiliação:
Estados Unidos