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Green tea (-)-epigallocatechin-3-gallate inhibits HGF-induced progression in oral cavity cancer through suppression of HGF/c-Met

Authors
 Yoon Woo Koh  ;  Eun Chang Choi  ;  Sung Un Kang  ;  Hye Sook Hwang  ;  Mi Hye Lee  ;  JungHee Pyun  ;  RaeHee Park  ;  YoungDon Lee  ;  Chul-Ho Kim 
Citation
 JOURNAL OF NUTRITIONAL BIOCHEMISTRY, Vol.22(11) : 1074-1083, 2011 
Journal Title
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
ISSN
 0955-2863 
Issue Date
2011
MeSH
Animals ; Catechin/analogs & derivatives* ; Catechin/pharmacology ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Chemoprevention ; Disease Progression ; Female ; Hepatocyte Growth Factor/antagonists & inhibitors* ; Humans ; KB Cells ; Matrix Metalloproteinase 2/biosynthesis ; Matrix Metalloproteinase 9/biosynthesis ; Mice ; Mouth Neoplasms/pathology ; Neoplasm Invasiveness ; Proto-Oncogene Proteins c-met/antagonists & inhibitors* ; Proto-Oncogene Proteins c-met/biosynthesis ; Signal Transduction/drug effects ; Tea
Keywords
HGF ; c-Met ; EGCG ; Tumor invasion ; Oral cancer ; Head and neck cancer
Abstract
Hepatocyte growth factor (HGF) and c-Met have recently attracted a great deal of attention as prognostic indicators of patient outcome, and they are important in the control of tumor growth and invasion. Epigallocatechin-3-gallate (EGCG) has been shown to modulate multiple signal pathways in a manner that controls the unwanted proliferation and invasion of cells, thereby imparting cancer chemopreventive and therapeutic effects. In this study, we investigated the effects of EGCG in inhibiting HGF-induced tumor growth and invasion of oral cancer in vitro and in vivo. We examined the effects of EGCG on HGF-induced cell proliferation, migration, invasion, induction of apoptosis and modulation of HGF/c-Met signaling pathway in the KB oral cancer cell line. We investigated the antitumor effect and inhibition of c-Met expression by EGCG in a syngeneic mouse model (C3H/HeJ mice, SCC VII/SF cell line). HGF promoted cell proliferation, migration, invasion and induction of MMP (matrix metalloproteinase)-2 and MMP-9 in KB cells. EGCG significantly inhibited HGF-induced phosphorylation of Met and cell growth, invasion and expression of MMP-2 and MMP-9. EGCG blocked HGF-induced phosphorylation of c-Met and that of the downstream kinases AKT and ERK, and inhibition of p-AKT and p-ERK by EGCG was associated with marked increases in the phosphorylation of p38, JNK, cleaved caspase-3 and poly-ADP-ribose polymerase. In C3H/HeJ syngeneic mice, as an in vivo model, tumor growth was suppressed and apoptosis was increased by EGCG. Our results suggest that EGCG may be a potential therapeutic agent to inhibit HGF-induced tumor growth and invasion in oral cancer.
Full Text
http://www.sciencedirect.com/science/article/pii/S0955286310002329
DOI
10.1016/j.jnutbio.2010.09.005
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers
Yonsei Authors
Koh, Yoon Woo(고윤우)
Choi, Eun Chang(최은창)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/94547
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