ArticleOncotarget2015
Elevated Src family kinase activity stabilizes E-cadherin-based junctions and collective movement of head and neck squamous cell carcinomas.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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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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
20 citing papers in PubMed, 28 citations in OpenAlex.
- Dasatinib suppresses collective cell migration through the coordination of focal adhesion andHeliyon · 2024Article
- Epithelial to Mesenchymal Transition: Key Regulator of Pancreatic Ductal Adenocarcinoma Progression and Chemoresistance.Cancers · 2021Review
- Partial EMT in Squamous Cell Carcinoma: A Snapshot.International journal of biological sciences · 2021Review
- Mucosal Epithelial Jak Kinases in Health and Diseases.Mediators of inflammation · 2021Review
- PEP06 polypeptide 30 is a novel cluster-dissociating agent inhibitingActa pharmaceutica Sinica. B · 2019Article
- The Differential Impact of SRC Expression on the Prognosis of Patients with Head and Neck Squamous Cell Carcinoma.Cancers · 2019Article
- Coordination of protrusion dynamics within and between collectively migrating border cells by myosin II.Molecular biology of the cell · 2019Article
- Stromal fibroblasts induce metastatic tumor cell clusters via epithelial-mesenchymal plasticity.Life science alliance · 2019Article
- Metastasis as a systemic disease: molecular insights and clinical implications.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- Collective cell migration and metastases induced by an epithelial-to-mesenchymal transition in Drosophila intestinal tumors.Nature communications · 2019Article
- The Emerging Link between Centrosome Aberrations and Metastasis.Developmental cell · 2019Review
- Combined inhibition of PI3K and Src kinases demonstrates synergistic therapeutic efficacy in clear-cell renal carcinoma.Oncotarget · 2018Article
- Redistribution of Adhesive Forces through Src/FAK Drives Contact Inhibition of Locomotion in Neural Crest.Developmental cell · 2018Article
- Recent advances in understanding the complexities of metastasis.F1000Research · 2018Review
- Janus kinase 3 regulates adherens junctions and epithelial mesenchymal transition through β-catenin.The Journal of biological chemistry · 2017Article
- Review
- Fibronectin-guided migration of carcinoma collectives.Nature communications · 2017Article
- Adherens Junction and E-Cadherin complex regulation by epithelial polarity.Cellular and molecular life sciences : CMLS · 2016Review
- Src promotes cutaneous wound healing by regulating MMP-2 through the ERK pathway.International journal of molecular medicine · 2016Article
- Application of functional vincristine plus dasatinib liposomes to deletion of vasculogenic mimicry channels in triple-negative breast cancer.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EGF receptor (EGFR) overexpression is thought to drive head and neck carcinogenesis however clinical responses to EGFR-targeting agents have been modest and alternate targets are actively sought to improve results. Src family kinases (SFKs), reported to act downstream of EGFR are among the alternative targets for which increased expression or activity in epithelial tumors is commonly associated to the dissolution of E-cadherin-based junctions and acquisition of a mesenchymal-like phenotype. Robust expression of total and activated Src was observed in advanced stage head and neck tumors (N=60) and in head and neck squamous cell carcinoma lines. In cultured cancer cells Src co-localized with E-cadherin in cell-cell junctions and its phosphorylation on Y419 was both constitutive and independent of EGFR activation. Selective inhibition of SFKs with SU6656 delocalized E-cadherin and disrupted cellular junctions without affecting E-cadherin expression and this effect was phenocopied by knockdown of Src or Yes. These findings reveal an EGFR-independent role for SFKs in the maintenance of intercellular junctions, which likely contributes to the cohesive invasion E-cadherin-positive cells in advanced tumors. Further, they highlight the need for a deeper comprehension of molecular pathways that drive collective cell invasion, in absence of mesenchymal transition, in order to combat tumor spread.
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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.