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Genistein and biochanin A inhibit the growth of human prostate cancer cells but not epidermal growth factor receptor tyrosine autophosphorylation
Author(s) -
Peterson Greg,
Barnes Stephen
Publication year - 1993
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.2990220408
Subject(s) - autophosphorylation , genistein , lncap , tyrosine kinase , epidermal growth factor , biochanin a , daidzein , endocrinology , medicine , receptor tyrosine kinase , tyrosine kinase inhibitor , epidermal growth factor receptor , biology , cancer research , receptor , microbiology and biotechnology , cancer cell , phosphorylation , cancer , protein kinase a
The effect of the isoflavones, genistein, daidzein, and biochanin A on the growth of the LNCaP and DU‐145 human prostate cancer cell lines has been examined. Genistein and biochanin A, but not daidzein, inhibit both serum and EGF‐stimulated growth of LNCaP and DU‐145 cells (IC50 values from 8.0 to 27 μg/ml for serum and 4.3 to 15 μg/ml for EGF), but have no significant effect of the EGF receptor tyrosine autophosphorylation. In contrast, tyrphostin 25, a specific EGF receptor tyrosine kinase inhibitor, inhibits EGF‐stimulated growth and EGF receptor tyrosine autophosphorylation in these whole cells, but does not inhibit serum‐stimulated growth. These data suggest that the mechanism of action of genistein and biochanin A does not depend on inhibition of EGF receptor tyrosine autophosphorylation, but on a more distal event in the EGF receptor‐mediated signal transduction cascade. © 1993 Wiley‐Liss, Inc.