Direct inhibition of insulin-like growth factor-I receptor kinase activity by (-)-epigallocatechin-3-gallate regulates cell transformation

Ming Li, Zhiwei He, Svetlana Ermakova, Duo Zheng, Faqing Tang, Yong Yeon Cho, Feng Zhu, Wei-Ya Ma, Yuk Y Sham, Evgeny A. Rogozin, Ann M. Bode, Ya Cao, Zigang Dong

Research output: Contribution to journalArticlepeer-review

107 Scopus citations

Abstract

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 (IC 50 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 down-stream 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.

Original languageEnglish (US)
Pages (from-to)598-605
Number of pages8
JournalCancer Epidemiology Biomarkers and Prevention
Volume16
Issue number3
DOIs
StatePublished - Mar 2007

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