ArticleOncogene2013
Mutant p53 enhances MET trafficking and signalling to drive cell scattering and invasion.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 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
123 citing papers in PubMed, 198 citations in OpenAlex.
- Trial
- Endoplasmic reticulum stress in brain metastatic cascade.NPJ precision oncology · 2026Review
- Δ133p53 isoform enhances TLR4 function to promote tumor growth.Carcinogenesis · 2025Article
- Distinct functional heterogeneity of TP53 R175 mutations in platinum-resistant ovarian cancer: unveiling molecular mechanisms and therapeutic targets.Cell death & disease · 2025Article
- Molecular targets and therapies associated with poor prognosis of triple‑negative breast cancer (Review).International journal of oncology · 2025Review
- A Phase Ia/b study of MEK1/2 inhibitor binimetinib with MET inhibitor crizotinib in patients with RAS mutant advanced colorectal cancer (MErCuRIC).BMC cancer · 2025Article
- From regulation to deregulation of p53 in hematologic malignancies: implications for diagnosis, prognosis and therapy.Biomarker research · 2024Review
- The MET Oncogene: An Update on Targeting Strategies.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Targeting mutant p53: a key player in breast cancer pathogenesis and beyond.Cell communication and signaling : CCS · 2024Review
- Cell fate regulation governed by p53: Friends or reversible foes in cancer therapy.Cancer communications (London, England) · 2024Review
- microRNA-205 represses breast cancer metastasis by perturbing the rab coupling protein [RCP]-mediated integrin β1 recycling on the membrane.Apoptosis : an international journal on programmed cell death · 2024Article
- Multi-omics analysis-based clinical and functional significance of a novel prognostic and immunotherapeutic gene signature derived from amino acid metabolism pathways in lung adenocarcinoma.Frontiers in immunology · 2024Article
- Mutant p53-ENTPD5 control of the calnexin/calreticulin cycle: a druggable target for inhibiting integrin-α5-driven metastasis.Journal of experimental & clinical cancer research : CR · 2023Article
- Common activities and predictive gene signature identified for genetic hypomorphs ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Increased Expression of the Δ133p53β Isoform Enhances Brain Metastasis.International journal of molecular sciences · 2023Article
- The dual role of p63 in cancer.Frontiers in oncology · 2023Review
- Li-Fraumeni Syndrome: Mutation ofCancers · 2022Review
- Effect of KRAS mutations and p53 expression on the postoperative prognosis of patients with colorectal cancer.Molecular genetics & genomic medicine · 2022Article
- Mutant p53: it's not all one and the same.Cell death and differentiation · 2022Review
- Cross-talk between mutant p53 and p62/SQSTM1 augments cancer cell migration by promoting the degradation of cell adhesion proteins.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
63 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
Abstract
Tumour-derived mutant p53 proteins promote invasion, in part, by enhancing Rab coupling protein (RCP)-dependent receptor recycling. Here we identified MET as an RCP-binding protein and showed that mutant p53 promoted MET recycling. Mutant p53-expressing cells were more sensitive to hepatocyte growth factor, the ligand for MET, leading to enhanced MET signalling, invasion and cell scattering that was dependent on both MET and RCP. In cells expressing the p53 family member TAp63, inhibition of TAp63 also lead to cell scattering and MET-dependent invasion. However, in cells that express very low levels of TAp63, the ability of mutant p53 to promote MET-dependent cell scattering was independent of TAp63. Taken together, our data show that mutant p53 can enhance MET signalling to promote cell scattering and invasion through both TAp63-dependent and -independent mechanisms. MET has a predominant role in metastatic progression and the identification of mechanisms through which mutations in p53 can drive MET signalling may help to identify and direct therapy.
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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.