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Isoflavone‐induced activation of extracellular signal‐regulated kinase (ERK 1/2) in non‐tumorigenic prostate epithelial cells
Author(s) -
Clubbs Elizabeth,
Bomser Joshua A
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1014-b
Subject(s) - glycitein , daidzein , genistein , equol , cancer research , prostate cancer , mapk/erk pathway , isoflavones , endocrinology , medicine , tyrosine kinase , prostate , signal transduction , biology , chemistry , microbiology and biotechnology , cancer
Epidemiological and experimental evidence suggests that increased consumption of soy is associated with a reduced risk for prostate cancer. Soy isoflavones are thought to be responsible, in part, for this anticancer activity. The present study evaluated the ability of four isoflavones (genistein, daidzein, glycitein, and equol) to modulate ERK1/2 activity in a non‐tumorigenic prostate epithelial cell line (RWPE‐1). ERK1/2 activity is associated with cellular proliferation and differentiation; however, the specific role of this pathway in prostate carcinogenesis is unknown. Treatment of cells with genistein, daidzein, equol, and glycitein (10μM) increased ERK1/2 activity 7.2, 7.3, 12.3, and 47‐fold respectively (p<0.05), as measured by immunoblot. Isoflavone‐induced ERK1/2 activation was both time and concentration dependent. Further characterization of glycitein‐induced ERK1/2 activation suggests involvement of vascular endothelial and epithelial growth factor receptor tyrosine kinase activity. Interestingly, isoflavone‐induced ERK1/2 activation was not observed in the highly malignant PC‐3 prostate epithelial cell line. These data suggest that glycitein, despite its relatively low abundance, is a potent activator of the ERK1/2 signaling cascade in prostate epithelial cells. Funded by USDA IFAFS.