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Modulation of E-cadherin by hepatocyte growth factor induces aggressiveness of gastric carcinoma

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Authors
Han, Sang-Uk; Lee, Hwa-Young; Lee, Jae-Ho; Kim, Wook-Hwan; Nam, Hyunja; Kim, Hong; Cho, Yong-Kwan; Kim, Myung-Wook; Lee, Kuhn Uk
Issue Date
2005-10-26
Publisher
Lippincott Williams and Wilkins
Citation
Ann Surg. 2005 Nov;242(5):676-83
Keywords
AdultAgedBiopsy, NeedleBlotting, WesternCadherins/drug effects/*metabolismCarcinoma/metabolism/pathology/surgeryCell ProliferationCohort StudiesFemaleHepatocyte Growth Factor/analysis/*metabolismHumansImmunohistochemistryMaleMiddle AgedNeoplasm Invasiveness/pathologyNeoplasm StagingProbabilityPrognosisSensitivity and SpecificityStomach Neoplasms/*metabolism/*pathology/surgeryTumor Cells, CulturedTumor Markers, Biological/*analysis/metabolism
Abstract
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.
ISSN
0003-4932 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=16244541

http://hdl.handle.net/10371/15922
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College of Medicine/School of Medicine (의과대학/대학원)Surgery (외과학전공)Journal Papers (저널논문_외과학전공)
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