하인두 편평세포암주의 증식과 침습을 유도하는 간세포성장인자에 대한 녹차추출물 억제효과 (Green Tea Extracts Inhibits HGF-Induced HNSCC Progression in vitro)

서지정보

· 발행기관 : 대한이비인후과학회
· 수록지 정보 : 대한이비인후-두경부외과학회지 / 51권 / 2호 / 163 ~ 170페이지
· 저자명 : 김철호, 임혜진, 강성운, 이하늘, 황혜숙, 윤용로, 김동현

초록

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 and
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 μM, EGCG 10 μM, HGF 10+EGCG 1 μM,
HGF 10+EGCG 10 μM. 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 μM, HGF 10+EGCG 10 μM 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).
Conclusion：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. (Korean J Otorhinolaryngol-
Head Neck Surg 2008;51:163-70)

영어초록

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 and
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 μM, EGCG 10 μM, HGF 10+EGCG 1 μM,
HGF 10+EGCG 10 μM. 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 μM, HGF 10+EGCG 10 μM 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).
Conclusion：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. (Korean J Otorhinolaryngol-
Head Neck Surg 2008;51:163-70)

참고자료

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