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Cancer Prevention Effect of Epigallocatechin-3-gallate through Regulate in C-terminal Src Kinase (CSK) Signaling Pathway  

Kim, Dae Yong (Department of Pharmaceutical Science & Engineering, Seowon University)
Choi, Bu Young (Department of Pharmaceutical Science & Engineering, Seowon University)
Publication Information
Korean Journal of Pharmacognosy / v.45, no.2, 2014 , pp. 127-134 More about this Journal
Abstract
A great interest is emerging about green tea as a tool against human cancer proliferation or inflammation, as pointed out by recent reports describing the inhibitory action of epigallocatechin gallate (EGCG) on angiogenesis, urokinase, metalloproteinases, and induction of inducible nitric oxide synthase. We proposed that EGCG may regulate a multi target signaling having wider spectra of action than those actions of single enzymes. CSK (c-terminal Src kinase) protein is a non-receptor tyrosine kinase involved in the cross-talk and mediation of many signaling pathways that promote cell proliferation, adhesion, invasion, migration, and tumorigenesis. Based on the knowledge that CSK activation is important for cancer proliferation we hypothesized that CSK could be a target of EGCG. Here we showed that EGCG effectively suppressed the growth of CSK MEF cell when compare with CSK knockout MEF cell growth. These results indicate that EGCG could be used as a chemoprevention to modulate CSK signal pathway in inflammatory processes and tumor formation.
Keywords
EGCG; c-Terminal Src kinase; CSK knockout MEF; Inflammation; tumor;
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