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Epigallocatechin-3-gallate inhibits paracrine and autocrine hepatocyte growth factor/scatter factor-induced tumor cell migration and invasion.

Authors
Kwak, IH; Shin, YH; Kim, M; Cha, HY; Nam, HJ; Lee, BS; Chaudhary, SC; Pai, KS; Lee, JH
Citation
Experimental & molecular medicine, 43(2):111-120, 2011
Journal Title
Experimental & molecular medicine
ISSN
1226-36132092-6413
Abstract
Aberrant activation of hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, Met, is involved in the development and progression of many human cancers. In the cell-based screening assay, (-)epigallocatechin-3-gallate (EGCG) inhibited HGF/SF-Met signaling as indicated by its inhibitory activity on HGF/SF-induced cell scattering and uPA activation (IC50=15.8 microgram/ml). Further analysis revealed that EGCG at low doses specifically inhibited HGF/SF-induced tyrosine phosphorylation of Met but not epidermal growth factor (EGF)-induced phosphorylation of EGF receptor (EGFR). On the other hand, high-dose EGCG decreased both Met and EGFR proteins. We also found that EGCG did not act on the intracellular portion of Met receptor tyrosine kinase, i.e., it inhibited InlB-dependent activation of Met but not NGF-induced activation of Trk-Met hybrid receptor. This inhibition decreased HGF-induced migration and invasion by parental or HGF/SF-transfected B16F10 melanoma cells in vitro in either a paracrine or autocrine manner. Furthermore, EGCG inhibited the invasion/metastasis of HGF/SF-transfected B16F10 melanoma cells in mice. Our data suggest the possible use of EGCG in human cancers associated with dysregulated paracrine or autocrine HGF/SF-Met signaling.
MeSH terms
AnimalsAutocrine Communication/*drug effectsCatechin/*analogs & derivatives/metabolism/pharmacologyCell Line, TumorCell Movement/drug effectsFemale*Hepatocyte Growth FactorHumansMiceMice, Inbred BALB CNeoplasms, Experimental/*metabolism/pathologyParacrine Communication/*drug effectsPhosphorylation/drug effectsProto-Oncogene Proteins c-met/antagonists & inhibitors/metabolismReceptors, Growth Factor/antagonists & inhibitors/metabolismSignal Transduction
DOI
10.3858/emm.2011.43.2.013
PMID
21209554
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pediatrics & Adolescent Medicine
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
AJOU Authors
김, 명덕배, 기수이, 재호
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