ArticleOncogene2007
A positive feedback loop between hepatocyte growth factor receptor and beta-catenin sustains colorectal cancer cell invasive growth.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 113 citations in OpenAlex.
- Molecular imaging tracers targeting c-MET: a systematic review of preclinical evidence and clinical translation.European journal of nuclear medicine and molecular imaging · 2026Review
- SPARC Promotes Corneal Epithelial Wound Healing Through β-catenin Nuclear Translocation and c-Met Activation.Investigative ophthalmology & visual science · 2026Article
- G Protein-Coupled Receptor Signaling: Implications and Therapeutic Development Advances in Cancers.MedComm · 2025Review
- Cancer-associated loss-of-function mutations in KCNQ1 enhance Wnt/β-catenin signalling disrupting epithelial homeostasis.Oncogene · 2025Article
- Review
- Taking the road less traveled - the therapeutic potential of CBP/β-catenin antagonists.Expert opinion on therapeutic targets · 2021Review
- Insulin-Like Growth Factor 2 mRNA-Binding Protein 1 (IGF2BP1) Is a Prognostic Biomarker and Associated with Chemotherapy Responsiveness in Colorectal Cancer.International journal of molecular sciences · 2021Article
- The utility of c-Met as a diagnostic tissue biomarker in primary colorectal cancer.International journal of experimental pathology · 2021Article
- Portrait of Cancer Stem Cells on Colorectal Cancer: Molecular Biomarkers, Signaling Pathways and miRNAome.International journal of molecular sciences · 2021Review
- Pharmacologically Targeting the WNT/β-Catenin Signaling Cascade: Avoiding the Sword of Damocles.Handbook of experimental pharmacology · 2021Article
- Receptor Tyrosine Kinases and Their Signaling Pathways as Therapeutic Targets of Curcumin in Cancer.Frontiers in pharmacology · 2021Review
- A Framework of Major Tumor-Promoting Signal Transduction Pathways Implicated in Melanoma-Fibroblast Dialogue.Cancers · 2020Review
- Wnt Signaling and Its Significance Within the Tumor Microenvironment: Novel Therapeutic Insights.Frontiers in immunology · 2019Review
- Wnt/β-Catenin Signaling as a Molecular Target by Pathogenic Bacteria.Frontiers in immunology · 2019Review
- Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) in cancer.Journal of hematology & oncology · 2018Review
- Wnt/β-Catenin Signaling and Obesity.Frontiers in physiology · 2018Review
- IMPs: an RNA-binding protein family that provides a link between stem cell maintenance in normal development and cancer.Genes & development · 2016Review
- Wnt Signaling in Cancer Stem Cell Biology.Cancers · 2016Review
- The evolving roles of canonical WNT signaling in stem cells and tumorigenesis: implications in targeted cancer therapies.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Decorin as a multivalent therapeutic agent against cancer.Advanced drug delivery reviews · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpressed or activated hepatocyte growth factor receptor, encoded by the MET proto-oncogene, was found in the majority of colorectal carcinomas (CRCs), whose stepwise progression to malignancy requires transcriptional activation of beta-catenin. We here demonstrate that a functional crosstalk between Met and beta-catenin signaling sustains and increases CRC cell invasive properties. Hepatocyte growth factor (HGF) stimulation prompts beta-catenin tyrosine phosphorylation and dissociation from Met, and upregulates beta-catenin expression via the phosphatidylinositol 3-kinase pathway in conditions that mimic those found by the invading and metastasizing cells. Additionally, a transcriptionally active form of beta-catenin, known to be oncogenic, enhances Met expression. Furthermore, HGF treatment increases the activity of the beta-catenin-regulated T-cell factor transcription factor in cells expressing the wild-type or the oncogenic beta-catenin. In the mirror experiments, either Met or beta-catenin knocking down also reduces their protein level. In biological assays, beta-catenin knocking down abrogates the HGF-induced motile phenotype, whereas active beta-catenin fosters ligand-independent cell scattering. Met and beta-catenin also cooperate in promoting entry into the cell cycle and in protecting cells from apoptosis. In conclusion, Met and beta-catenin pathways are mutually activated in CRC cells. This might generate a self-amplifying positive feedback loop resulting in the upregulation of the invasive growth properties of CRC cells.
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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.