ArticlePloS one2014
Reciprocal activating crosstalk between c-Met and caveolin 1 promotes invasive phenotype in hepatocellular carcinoma.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 32 citations in OpenAlex.
- A Novel Zebrafish Liver-Specific Metastasis Model Reveals c-Met as a Driver of Liver Tropism.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- Inhibition of the Caveolin-1 pathway promotes apoptosis and overcomes pan-tyrosine kinase inhibitor resistance in hepatocellular carcinoma.Cell death & disease · 2025Article
- [Research progress on the involvement of exosome-mediated intercellular communication in the remodeling and the regulation of invasion and metastasis in the hepatocellular tumor microenvironment].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025Review
- The Emerging Role of c-Met in Carcinogenesis and Clinical Implications as a Possible Therapeutic Target.Journal of oncology · 2022Review
- Role of Biobanks for Cancer Research and Precision Medicine in Hepatocellular Carcinoma.Journal of gastrointestinal cancer · 2021Review
- CXCR4 promotes gefitinib resistance of Huh7 cells by activating the c-Met signaling pathway.FEBS open bio · 2021Article
- High glucose induced c-Met activation promotes aggressive phenotype and regulates expression of glucose metabolism genes in HCC cells.Scientific reports · 2021Article
- lncRNA HOTAIR overexpression induced downregulation of c-Met signaling promotes hybrid epithelial/mesenchymal phenotype in hepatocellular carcinoma cells.Cell communication and signaling : CCS · 2020Article
- AXL and CAV-1 play a role for MTH1 inhibitor TH1579 sensitivity in cutaneous malignant melanoma.Cell death and differentiation · 2020Article
- HGF/c-Met Axis: The Advanced Development in Digestive System Cancer.Frontiers in cell and developmental biology · 2020Review
- Tumorigenesis, diagnosis, and therapeutic potential of exosomes in liver cancer.Journal of hematology & oncology · 2019Review
- Association of caveolin-1 protein expression with hepatocellular carcinoma: a meta-analysis and literature review.Cancer management and research · 2019Article
- Role of caveolin-1 in hepatocellular carcinoma arising from non-alcoholic fatty liver disease.Cancer science · 2018Article
- The Chemokine Receptor CXCR4 and c-MET Cooperatively Promote Epithelial-Mesenchymal Transition in Gastric Cancer Cells.Translational oncology · 2018Article
- Signaling Pathways as Potential Therapeutic Targets in Hepatocarcinogenesis.Journal of gastrointestinal cancer · 2017Review
- The different functions and clinical significances of caveolin-1 in human adenocarcinoma and squamous cell carcinoma.OncoTargets and therapy · 2017Review
- Elevated hepatocyte growth factor expression as an autocrine c-Met activation mechanism in acquired resistance to sorafenib in hepatocellular carcinoma cells.Cancer science · 2016Article
- Apoptosis in liver carcinogenesis and chemotherapy.Hepatic oncology · 2015Review
- c-Met and Other Cell Surface Molecules: Interaction, Activation and Functional Consequences.Biomedicines · 2015Review
- c-MET receptor tyrosine kinase as a molecular target in advanced hepatocellular carcinoma.Journal of hepatocellular carcinoma · 2015Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-Met, the receptor for Hepatocyte Growth Factor (HGF), overexpressed and deregulated in Hepatocellular Carcinoma (HCC). Caveolin 1 (CAV1), a plasma membrane protein that modulates signal transduction molecules, is also overexpressed in HCC. The aim of this study was to investigate biological and clinical significance of co-expression and activation of c-Met and CAV1 in HCC. We showed that c-Met and CAV1 were co-localized in HCC cells and HGF treatment increased this association. HGF-triggered c-Met activation caused a concurrent rise in both phosphorylation and expression of CAV1. Ectopic expression of CAV1 accelerated c-Met signaling, resulted in enhanced migration, invasion, and branching-morphogenesis. Silencing of CAV1 downregulated c-Met signaling, and decreased migratory/invasive capability of cells and attenuated branching morphogenesis. In addition, activation and co-localization of c-Met and CAV1 were elevated during hepatocarcinogenesis. In conclusion reciprocal activating crosstalk between c-Met and CAV1 promoted oncogenic signaling of c-Met contributed to the initiation and progression of HCC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.