OBJECTIVE: Hepatocyte growth factor (HGF) is well known as a scatter factor because it can disperse cells. E-cadherin is a protein that plays a main role in the establishment of cell-cell adhesion. This study focused on the role of HGF on the expression and distribution of E-cadherin. Furthermore, we found induction of aggressiveness of gastric carcinoma by modulation of E-cadherin by HGF. MATERIALS AND METHODS: Tumor tissues from 50 patients with gastric carcinoma were evaluated for the expression of HGF, its receptor c-Met, and E-cadherin. Western blot analysis and invasion assay were performed to confirm the role of HGF on the modulation of E-cadherin using human gastric cancer cell lines. RESULTS: Seventy-eight percent of the gastric carcinoma tissues showed overexpression of c-Met. E-cadherin expression was found in 86%, which could be further classified as membranous type (52%) or nonmembranous type (48%). The levels of HGF in tumor tissues increased significantly according to the tumor progression. The levels of HGF in tumors with nonmembranous type E-cadherin expression were significantly higher than those in tumors with membranous expression. A striking morphologic change from epithelial shape to fibroblastic shape was observed in SNU-16 cells after 3 days' exposure to HGF, accompanied by down-regulation of functional E-cadherin in the membrane. Treatment of the cells with HGF induced significant invasion into the matrigel. CONCLUSION: We can conclude that HGF can modulate the expression of E-cadherin in gastric carcinoma, which was accompanied by more aggressive phenotype.
OBJECTIVE:Hepatocyte growth factor (HGF) is well known as a scatter factor because it can disperse cells. E-cadherin is a protein that plays a main role in the establishment of cell-cell adhesion. This study focused on the role of HGF on the expression and distribution of E-cadherin. Furthermore, we found induction of aggressiveness of gastric carcinoma by modulation of E-cadherin by HGF. MATERIALS AND METHODS:Tumor tissues from 50 patients with gastric carcinoma were evaluated for the expression of HGF, its receptor c-Met, and E-cadherin. Western blot analysis and invasion assay were performed to confirm the role of HGF on the modulation of E-cadherin using humangastric cancer cell lines. RESULTS: Seventy-eight percent of the gastric carcinoma tissues showed overexpression of c-Met. E-cadherin expression was found in 86%, which could be further classified as membranous type (52%) or nonmembranous type (48%). The levels of HGF in tumor tissues increased significantly according to the tumor progression. The levels of HGF in tumors with nonmembranous type E-cadherin expression were significantly higher than those in tumors with membranous expression. A striking morphologic change from epithelial shape to fibroblastic shape was observed in SNU-16 cells after 3 days' exposure to HGF, accompanied by down-regulation of functional E-cadherin in the membrane. Treatment of the cells with HGF induced significant invasion into the matrigel. CONCLUSION: We can conclude that HGF can modulate the expression of E-cadherin in gastric carcinoma, which was accompanied by more aggressive phenotype.
Authors: J H Lee; S U Han; H Cho; B Jennings; B Gerrard; M Dean; L Schmidt; B Zbar; G F Vande Woude Journal: Oncogene Date: 2000-10-12 Impact factor: 9.867
Authors: D S Grant; H K Kleinman; I D Goldberg; M M Bhargava; B J Nickoloff; J L Kinsella; P Polverini; E M Rosen Journal: Proc Natl Acad Sci U S A Date: 1993-03-01 Impact factor: 11.205
Authors: D P Bottaro; J S Rubin; D L Faletto; A M Chan; T E Kmiecik; G F Vande Woude; S A Aaronson Journal: Science Date: 1991-02-15 Impact factor: 47.728
Authors: F Bussolino; M F Di Renzo; M Ziche; E Bocchietto; M Olivero; L Naldini; G Gaudino; L Tamagnone; A Coffer; P M Comoglio Journal: J Cell Biol Date: 1992-11 Impact factor: 10.539