Effect of Hepatocyte Growth Factor on the Expression of E-cadherin in Gastric Carcinoma Cell Lines.
- Author:
Sang Uk HAN
1
;
Won Hung LEE
;
Wook Hwan KIM
;
Myung Wook KIM
;
Jae Ho LEE
;
Sang Yong SONG
;
Kuhn Uk LEE
Author Information
1. Departments of Surgery, School of Medicine, Ajou University, Suwon, Korea. hansu@madang.ajou.ac.kr
- Publication Type:Original Article
- Keywords:
Stomach neoplasm;
Hepatocyte growth factor;
c-Met gene;
E-cadherin;
Invasion
- MeSH:
Blotting, Western;
Cadherins*;
Cell Adhesion;
Cell Fractionation;
Cell Line*;
Cell Proliferation;
Cytoplasm;
Fibroblasts;
gamma Catenin;
Hand;
Hepatocyte Growth Factor*;
Hepatocytes*;
Immunoprecipitation;
Membranes;
Phosphorylation;
Stomach Neoplasms;
Tyrosine
- From:Journal of the Korean Cancer Association
2000;32(5):852-862
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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, alpha-, beta-, gamma-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.
