ArticleAnnals of surgery2005
Modulation of E-cadherin by hepatocyte growth factor induces aggressiveness of gastric carcinoma.
Article in Annals of surgery, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- C-Met as a prognostic marker in gastric cancer: a systematic review and meta-analysis.PloS one · 2013Pooled it
- Lidocaine suppresses the malignant behavior of gastric cancer cells via the c-Met/c-Src pathway.Experimental and therapeutic medicine · 2021Article
- Crosstalk Between Cancer Associated Fibroblasts and Cancer Cells in Scirrhous Type Gastric Cancer.Frontiers in oncology · 2020Review
- Direct targeting of HGF by miR-16 regulates proliferation and migration in gastric cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Clinicopathological Significance and Diagnostic Accuracy of c-MET Expression by Immunohistochemistry in Gastric Cancer: A Meta-Analysis.Journal of gastric cancer · 2016Article
- Gelsolin-mediated activation of PI3K/Akt pathway is crucial for hepatocyte growth factor-induced cell scattering in gastric carcinoma.Oncotarget · 2016Article
- Clinical significance of MET in gastric cancer.World journal of gastrointestinal oncology · 2015Review
- PRMT1 Is a Novel Regulator of Epithelial-Mesenchymal-Transition in Non-small Cell Lung Cancer.The Journal of biological chemistry · 2015Article
- Clinical significance of hepatocyte growth factor/c-Met expression in the assessment of gastric cancer progression.Molecular medicine reports · 2015Article
- Clinical impact of the HGF/MET pathway activation in patients with advanced gastric cancer treated with palliative chemotherapy.The pharmacogenomics journal · 2014Article
- Combined γ-tocotrienol and Met inhibitor treatment suppresses mammary cancer cell proliferation, epithelial-to-mesenchymal transition and migration.Cell proliferation · 2013Article
- Plexin B1 inhibits MET through direct association and regulates Shp2 expression in melanocytes.Journal of cell science · 2013Article
- Lentivirus-mediated RNA silencing of c-Met markedly suppresses peritoneal dissemination of gastric cancer in vitro and in vivo.Acta pharmacologica Sinica · 2012Article
- Sema4D, the ligand for Plexin B1, suppresses c-Met activation and migration and promotes melanocyte survival and growth.The Journal of investigative dermatology · 2012Article
- Beta-catenin signaling involves HGF-enhanced HepG2 scattering through activating MMP-7 transcription.Histochemistry and cell biology · 2010Article
- Effects of atmospheric nonthermal plasma on invasion of colorectal cancer cells.Applied physics letters · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveHepatocyte 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
methodsTumor 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.
resultsSeventy-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.
conclusionWe can conclude that HGF can modulate the expression of E-cadherin in gastric carcinoma, which was accompanied by more aggressive phenotype.
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Registered trials
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