ArticleCancer research2013
CTEN prolongs signaling by EGFR through reducing its ligand-induced degradation.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 64 citations in OpenAlex.
- TNS1 and TNS4 play a potential role in development of pancreatic ductal adenocarcinoma but not TNS2 and TNS3.Cell adhesion & migration · 2026Article
- Tensins in Cancer: Integration of Their Domain Functions, Context-Dependent Regulation and Biomarker Potential.Biology · 2025Review
- Modeling the dynamics of EMT reveals genes associated with pan-cancer intermediate states and plasticity.NPJ systems biology and applications · 2025Article
- Hypoxia-driven TNS4 fosters HNSCC tumorigenesis by stabilizing integrin α5β1 complex and triggering FAK-mediated Akt and TGFβ signaling pathways.International journal of biological sciences · 2024Article
- The role of CBL family ubiquitin ligases in cancer progression and therapeutic strategies.Frontiers in pharmacology · 2024Review
- The postbiotic sodium butyrate synergizes the antiproliferative effects of dexamethasone against the AGS gastric adenocarcinoma cells.Frontiers in nutrition · 2024Article
- Predicting tumor repopulation through the gene panel derived from radiation resistant colorectal cancer cells.Journal of translational medicine · 2023Article
- Epigenetic Activation of Tensin 4 Promotes Gastric Cancer Progression.Molecules and cells · 2023Article
- The SMARCA4NPJ precision oncology · 2023Article
- The role of tensins in malignant neoplasms.Archives of medical science : AMS · 2023Article
- Article
- Immunohistochemical Analysis of the Expression of Adhesion Proteins: TNS1, TNS2 and TNS3 in Correlation with Clinicopathological Parameters in Gastric Cancer.Biomolecules · 2021Article
- PRMT1-mediated H4R3me2a recruits SMARCA4 to promote colorectal cancer progression by enhancing EGFR signaling.Genome medicine · 2021Article
- Tensins - emerging insights into their domain functions, biological roles and disease relevance.Journal of cell science · 2021Review
- CTEN Induces Tumour Cell Invasion and Survival and Is Prognostic in Radiotherapy-Treated Head and Neck Cancer.Cancers · 2020Article
- The miR-1224-5p/TNS4/EGFR axis inhibits tumour progression in oesophageal squamous cell carcinoma.Cell death & disease · 2020Article
- Article
- Molecular Pathogenesis of Gene Regulation by theCancers · 2019Article
- Identification of subcellular targeting sequences of Cten reveals its role in cell proliferation.Biochimica et biophysica acta. Molecular cell research · 2019Article
- Downregulation of C-Terminal Tensin-Like Protein (CTEN) Suppresses Prostate Cell Proliferation and Contributes to Acinar Morphogenesis.International journal of molecular sciences · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Activation of EGF receptor (EGFR) triggers signaling pathways regulating various cellular events that contribute to tissue development and function. Aberrant activation of EGFR contributes to tumor progression as well as therapeutic resistance in patients with cancer. C-terminal tensin-like (CTEN; TNS4) is a focal adhesion molecule that is a member of the tensin family. Its expression is upregulated by EGF and elevated CTEN mediates EGF-induced cell migration. In the presence of CTEN, we found that EGF treatment elevated the level of EGFR protein but not mRNA. The extended half-life of activated EGFR sustained its signaling cascades. CTEN reduced ligand-induced EGFR degradation by binding to the E3 ubiquitin ligase c-Cbl and decreasing the ubiquitination of EGFR. The Src homology 2 domain of CTEN is not only required for binding to the phosphorylated tyrosine residue at codon 774 of c-Cbl, but is also essential for the tumorigenicity observed in the presence of CTEN. Public database analyses indicated that CTEN mRNA levels are elevated in breast, colon, lung, and pancreas cancers, but not correlated with EGFR mRNA levels in these cancers. In contrast, immunohistochemistry analyses of lung cancer specimens showed that CTEN and EGFR protein levels were positively associated, in support of our finding that CTEN regulates EGFR protein levels through a posttranslational mechanism. Overall, this work defines a function for CTEN in prolonging signaling from EGFR by reducing its ligand-induced degradation.
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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.