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Direct Inhibition of Insulin-Like Growth Factor-I Receptor Kinase Activity by (–)–Epigallocatechin-3-Gallate Regulates Cell Transformation

¹ Hormel Institute, University of Minnesota, Austin, Minnesota; ² Computational Biology/Biochemistry Consultant, Supercomputing Institute, University of Minnesota, Minneapolis, Minnesota; and ³ Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha, Hunan, China

Requests for reprints: Zigang Dong, Hormel Institute, University of Minnesota, 801 16th Avenue Northeast, Austin, MN 55912. Phone: 507-437-9600; Fax: 507-437-9606. E-mail: zgdong{at}hi.umn.edu

Insulin-like growth factor-I receptor (IGF-IR) has been implicated in cancer pathophysiology. Furthermore, impairment of IGF-IR signaling in various cancer cell lines caused inhibition of the transformed phenotype as determined by the inhibition of colony formation in soft agar and the inhibition of tumor formation in athymic nude mice. Thus, the IGF-IR might be an attractive target for cancer prevention. We showed that the tea polyphenol, (–)–epigallocatechin-3-gallate (EGCG), is a small-molecule inhibitor of IGF-IR activity (IC₅₀ of 14 µmol/L). EGCG abrogated anchorage-independent growth induced by IGF-IR overexpression and also prevented human breast and cervical cancer cell phenotype expression through inhibition of IGF-IR downstream signaling. Our findings are the first to show that the IGF-IR is a novel binding protein of EGCG and thus may help explain the chemopreventive effect of EGCG on cancer development. (Cancer Epidemiol Biomarkers Prev 2007;16(3):598–605)

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