Cited 0 times in

64 2

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 ; Chul-Ho Kim ; YoungDon Lee ; RaeHee Park ; JungHee Pyun ; Mi Hye Lee ; Hye Sook Hwang ; Sung Un Kang 
Citation
 Journal of Nutritional Biochemistry, Vol.22(11) : 1074~1083, 2011 
Journal Title
 Journal of Nutritional Biochemistry 
ISSN
 0955-2863 
Issue Date
2011
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.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/94547
DOI
10.1016/j.jnutbio.2010.09.005
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Otorhinolaryngology
Yonsei Authors
사서에게 알리기
  feedback
Link
 http://www.sciencedirect.com/science/article/pii/S0955286310002329
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse