ArticleCancer science2008
Constitutive activation of c-Met is correlated with c-Met overexpression and dependent on cell-matrix adhesion in lung adenocarcinoma cell lines.
Article in Cancer science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- C-MET tyrosine kinase receptor: mechanisms, clinical applications and future perspectives in cancer therapy.Signal transduction and targeted therapy · 2026Review
- MET (c-Met) protein overexpression is an emerging protein biomarker in non-small cell lung cancer.NPJ precision oncology · 2025Review
- Targeting Heat Shock Transcription Factor 4 Enhances the Efficacy of Cabozantinib and Immune Checkpoint Inhibitors in Renal Cell Carcinoma.International journal of molecular sciences · 2025Article
- The PSI Domain of the MET Oncogene Encodes a Functional Disulfide Isomerase Essential for the Maturation of the Receptor Precursor.International journal of molecular sciences · 2022Article
- Review
- MET targeting: time for a rematch.Oncogene · 2020Review
- Met is involved in TIGAR-regulated metastasis of non-small-cell lung cancer.Molecular cancer · 2018Article
- Clinical impact of high serum hepatocyte growth factor in advanced non-small cell lung cancer.Oncotarget · 2017Article
- [Mechanism of c-MET in Non-small Cell Lung Cancer and Its Treatment and Testing].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2015Review
- Inhibition of ligand-independent constitutive activation of the Met oncogenic receptor by the engineered chemically-modified antibody DN30.Molecular oncology · 2015Article
- cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance.Cancers · 2015Review
- HGF/c-Met overexpressions, but not met mutation, correlates with progression of non-small cell lung cancer.Pathology oncology research : POR · 2012Article
- HGF Airway Over-expression Leads to Enhanced Pulmonary Vascularization without Induction of VEGF.Current angiogenesis · 2012Article
- Article
- Durable complete response of metastatic gastric cancer with anti-Met therapy followed by resistance at recurrence.Cancer discovery · 2011Article
- An overview of the c-MET signaling pathway.Therapeutic advances in medical oncology · 2011Article
- Growth factor signaling pathways as targets for prevention of epithelial carcinogenesis.Molecular carcinogenesis · 2011Review
- Ligand-independent activation of c-Met by fibronectin and α(5)β(1)-integrin regulates ovarian cancer invasion and metastasis.Oncogene · 2011Article
- Inhibition of c-Met downregulates TIGAR expression and reduces NADPH production leading to cell death.Oncogene · 2011Article
- Co-activation of epidermal growth factor receptor and c-MET defines a distinct subset of lung adenocarcinomas.The American journal of pathology · 2010Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study we explored the mechanisms of constitutive activation of c-Met in lung adenocarcinoma cell lines. First, we examined levels of c-Met and phospho-c-Met (Y1234/Y1235) in a panel of lung adenocarcinoma cell lines by Western blot analysis. c-Met expression was found in 12 of 14 cell lines and an overall correlation between the expressions of c-Met and phospho-c-Met was noted. c-Met was constitutively activated particularly at high levels in five cell lines (PC3, LC-2/ad, L27, H1648, and H2009). c-Met amplification was identified in L27 and H1648 by single nucleotide polymorphism array analysis, but no mutations were identified in the Sema domain or in any part of the cytoplasmic domain of c-Met. Experiments with neutralizing anti-hepatocyte growth factor (HGF) antibody, scatter assay using Madin-Darby canine kidney cells, and Western blotting on conditioned media of the cell lines revealed that the constitutive phosphorylation of c-Met was largely ligand-independent. The inhibition of cell-matrix adhesion induced the dephosphorylation of c-Met in the five cell lines tested. This was accompanied by downregulation of c-Met in three of the five cell lines. In contrast, the inhibition of cell-cell adhesion by neutralizing E-cadherin antibody had a minimal effect on the expression and phosphorylation of c-Met. These results reveal three features of the constitutive activation of c-Met in our panel of lung adenocarcinoma cell lines: (i) it correlates with c-Met overexpression, either with or without gene amplification; (ii) it is largely ligand-independent; and (iii) it depends on cell-matrix adhesion.
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