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

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dc.contributor.authorKoh, YW-
dc.contributor.authorChoi, EC-
dc.contributor.authorKang, SU-
dc.contributor.authorHwang, HS-
dc.contributor.authorLee, MH-
dc.contributor.authorPyun, J-
dc.contributor.authorPark, R-
dc.contributor.authorLee, Y-
dc.contributor.authorKim, CH-
dc.date.accessioned2012-05-04T01:03:12Z-
dc.date.available2012-05-04T01:03:12Z-
dc.date.issued2011-
dc.identifier.issn0955-2863-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/6761-
dc.description.abstractHepatocyte 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.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHCatechin-
dc.subject.MESHCell Movement-
dc.subject.MESHCell Proliferation-
dc.subject.MESHChemoprevention-
dc.subject.MESHDisease Progression-
dc.subject.MESHFemale-
dc.subject.MESHHepatocyte Growth Factor-
dc.subject.MESHHumans-
dc.subject.MESHKB Cells-
dc.subject.MESHMatrix Metalloproteinase 2-
dc.subject.MESHMatrix Metalloproteinase 9-
dc.subject.MESHMice-
dc.subject.MESHMouth Neoplasms-
dc.subject.MESHNeoplasm Invasiveness-
dc.subject.MESHProto-Oncogene Proteins c-met-
dc.subject.MESHSignal Transduction-
dc.subject.MESHTea-
dc.titleGreen tea (-)-epigallocatechin-3-gallate inhibits HGF-induced progression in oral cavity cancer through suppression of HGF/c-Met.-
dc.typeArticle-
dc.identifier.pmid21292466-
dc.identifier.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0955-2863(10)00232-9-
dc.contributor.affiliatedAuthor이, 영돈-
dc.contributor.affiliatedAuthor김, 철호-
dc.type.localJournal Papers-
dc.identifier.doi10.1016/j.jnutbio.2010.09.005-
dc.citation.titleThe Journal of nutritional biochemistry-
dc.citation.volume22-
dc.citation.number11-
dc.citation.date2011-
dc.citation.startPage1074-
dc.citation.endPage1083-
dc.identifier.bibliographicCitationThe Journal of nutritional biochemistry, 22(11). : 1074-1083, 2011-
dc.identifier.eissn1873-4847-
dc.relation.journalidJ009552863-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Anatomy
Journal Papers > School of Medicine / Graduate School of Medicine > Otolaryngology
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