Green Tea Extracts Inhibits HGF-Induced HNSCC Progression in vitro
하인두 편평세포암주의 증식과 침습을 유도하는 간세포성장인자에 대한 녹차추출물 억제효과
김, 철호; 임, 혜진; 강, 성운; 이, 하늘; 황, 혜숙; 윤, 용로; 김, 동현
Taehan Ibi Inhukwa Hakhoe chi, 51(2):163-170, 2008
Taehan Ibi Inhukwa Hakhoe chi; Journal of the Korean Otolaryngological Society; 대한이비인후과학회지
Background & Objectives: Aberrant activation of hepatocyte growth factor (HGF) and its receptor, c-Met, has been known to be involved in many human cancer development and progression. During the search for an effective molecule inhibitor of HGF/ c-Met signaling, we have found that Epigallocatechin-3-gallate (EGCG) in green tea might inhibit HGF/c-Met signaling. Studies were performed to address whether EGCG inhibited HGF-dependent tumor proliferation and invasion in HNSCC.
Materials & Method: For EGCG inhibition of HGF/c-Met signaling, Western blot was performed. The proliferation of FaDu cells was assayed by counting the number of the cells after treatment by HGF 0, 10 ng/ml, EGCG 1 micrometer, EGCG 10 micrometer, HGF 10+EGCG 1 micrometer, HGF 10+EGCG 10 micrometer. The dispersion of cells was observed by measuring the separation and morphologic changes of the cells after treatment with HGF 0, 10 ng/ml HGF 10+EGCG 1 micrometer, HGF 10+EGCG 10 micrometer for 24 hours. Tumor cell migration was assessed by wound healing assay and tumor cell invasiveness was assessed by the membrane invasion assay.
Results: HGF treatment induced rapid activation of c-Met and EGCG inhibited HGF-induced c-Met signaling in FaDu cells. HGF significantly enhanced the growth of HNSCC cells and this phenomenon was inhibited by EGCG in a dose-dependant manner (p<0.05). EGCG inhibited HGF-induced scattering, migration, and invasion of HNSCC cells in a dose-dependent manner (p<0.05).
Conclusions: Inhibition of HGF/Met by EGCG leads to decreased proliferation, scattering, migration and invasion in vitro, suggesting the possible use of EGCG in HNSCC associated with down-regulation of HGF/Met signaling.
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