Abstract Title:

Green tea (-)-epigalocatechin-3-gallate inhibits KIT activity and causes caspase-dependent cell death in gastrointestinal stromal tumor including imatinib-resistant cells.

Abstract Source:

Cancer Biol Ther. 2009 Oct;8(20):1934-9. Epub 2009 Oct 22. PMID: 19770581

Abstract Author(s):

Hoang Thanh Chi, Hoang Anh Vu, Reo Iwasaki, Le Ba Thao, Yukihiko Hara, Takahiro Taguchi, Toshiki Watanabe, Yuko Sato


Imatinib, a selective tyrosine kinase inhibitor, has been used as a standard first-line therapy for gastrointestinal stromal tumor (GIST) patients. Unfortunately, most patients responding to imatinib will eventually exhibit the resistance, the cause of which is not fully understood. The serious clinical problems of imatinib-resistance demand alternative treatment strategy. (-)-Epigallocatechin-3-gallate (EGCG), a main component of green tea catechin, has been demonstrated potential anti-tumor effects on various types of cancer cells. Here, we report for the first time that EGCG has shown anti-tumor effects on gastrointestinal stromal tumor cell line GIST-T1 by suppressing cell proliferation and eventually inducing cell death via caspase-dependent pathways. GIST-T1 and imatinib resistant GIST-T1 (GIST-T1 IR) cells were used to assess the effects of EGCG. In both cell types, KIT activity was completely inhibited after 4 h treatment with 60 muM EGCG. EGCG specifically inhibited activated KIT, which was demonstrated by using Ba/F3 cells transfected with human wild-type KIT construct. At a dose of 30 muM EGCG, the KIT activity remains but at more than 40 muM EGCG, the KIT activity was abolished in these transfected-Ba/F3 cells. Our results suggest that EGCG has a promising potential as a natural KIT inhibitor and therefore it could be used as a novel therapeutic or preventive reagent for GISTs including the imatinib-resistant cases.

Study Type : Animal Study

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