Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/7563
Title: Mechanism involved in genistein activation of insulin-like growth factor 1 receptor expression in human breast cancer cells
Authors: Chen, WF
Gao, QG
Wong, MS 
Keywords: Genistein
Oestrogen
Insulin-like growth factor 1 receptor
Oestrogen receptor
Human breast cancer
Issue Date: 1-Dec-2007
Publisher: Cambridge University Press
Source: British journal of nutrition, 1 Dec. 2007, v. 98, no. 6, p. 1120-1125 How to cite?
Journal: British journal of nutrition 
Abstract: Our previous studies have shown that genistein can enhance the insulin-like growth factor (IGF)-1 receptor signalling pathway via an oestrogen receptor (ER) in human breast cancer MCF-7 cells. The present study aims to investigate how genistein regulates IGF-1 receptor expression in human MCF-7 cells. Genistein at 1 μm stimulated the growth of MCF-7 cells and this effect could be completely blocked by the IGF-1 receptor antagonist JB-1, suggesting that IGF-1 receptor is essential for mediating the proliferative effects of genistein in MCF-7 cells. Genistein increased IGF-1 receptor promoter activity. This effect could be completely abolished by co-treatment of MCF-7 cells with ICI 182,780 (10− 6 m). Genistein increased IGF-1 receptor gene expression and this effect could be completely blocked by the IGF-1 receptor antagonist JB-1. Co-treatment of MCF-7 cells with cycloheximide (5 μg/ml) completely blocked the induction of IGF-1 receptor protein and mRNA expression by genistein. The results indicated that the induction of IGF-1 receptor promoter activity by genistein required the action of ER while the stimulatory actions of genistein on IGF-1 receptor expression required the activity of the IGF-1 receptor and de novo protein synthesis. These data provide evidence to support the hypothesis that the inductive effects of genistein on IGF-1 receptor expression require the cross-talk between IGF-1 receptor and the ER-dependent pathways.
URI: http://hdl.handle.net/10397/7563
ISSN: 0007-1145
EISSN: 1475-2662
DOI: 10.1017/S0007114507777139
Rights: © The Authors 2007. The journal web page is located at: http://journals.cambridge.org/action/displayJournal?jid=BJN
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