Effect of Hepatocyte Growth Factor on the Expression of E-cadherin in Gastric Carcinoma Cell Lines
위암세포주에서 간세포성장인자가 E-cadherin의 발현에 미치는 영향
한, 상욱; 이, 원흥; 김, 욱환; 김, 명욱; 이, 재호; 송, 상용; 이, 건욱
Taehan Am Hakhoe chi, 32(5):852-862, 2000
Taehan Am Hakhoe chi; Journal of Korean Cancer Association; 대한암학회지
Purpose :Previously, we reported that the expression of E-cadherin was significantly decreased according to the increase of the level of hepatocyte growth factor (HGF) in gastric cancer tissue. In this work, the effect of HGF on the cell-cell adhesion and intracellular distribution of E-cadherin in the gastric carcinoma cell lines were studied.
Materials and Methods :Western blot analysis was performed to confirm the presence or abscence of c-Met and E-cadherin in SNU-1, 5, and 16 cells. Tyrosine phosphorylation of c-Met, E-cadherin, α-, β-, γ-catenins was checked by immunoprecipitation. The morphologic changes induced by HGF were studied with immunocytochemical staining. Functional proportion of E-cadherin was estimated by cell fractionation. The effect of HGF on cell proliferation and invasion was also assessed.
Results :Among SNU-1, 5, and 16 cell lines, only SNU-16 cells expressed both E-cadherin and c-Met. A morphological change from epithelial shape to fibroblastic one was observed in the SNU-16 cells after treatment with HGF. In addition, E-cadherin expression of the SNU-16 cells was shifted from the membrane and to the cytoplasm, and the functional fraction of E-cadherin was decreased in the SNU-16 cells treated with HGF. On the other hand, HGF increased the proliferation and invasion of the SNU-16 cells.
Conclusion :These results suggest that HGF may regulate cell adhesion in gastric carcinomas via the cellular redistribution and functional change of E-cadherin.
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