ArticleOncotarget2015
Celecoxib increases EGF signaling in colon tumor associated fibroblasts, modulating EGFR expression and degradation.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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
9 citing papers in PubMed, 18 citations in OpenAlex.
- From microtubule remodeling to clinical translation: the multifaceted roles of vasohibin-1 in disease modulation.Frontiers in immunology · 2026Review
- Investigation of the Potential Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2023Article
- Reprogramming the tumor microenvironment to improve the efficacy of cancer immunotherapies.Medical oncology (Northwood, London, England) · 2022Review
- Effects of Cyclooxygenase-2 Inhibitors on Gastrointestinal Malignancies: a Systematic Review and Meta-analysis.Indian journal of surgical oncology · 2022Article
- Post-translational modifications of prostaglandin-endoperoxide synthase 2 in colorectal cancer: An update.World journal of gastroenterology · 2018Review
- TRAF6 regulates EGF-induced cell transformation and cSCC malignant phenotype through CD147/EGFR.Oncogenesis · 2018Article
- Targeting the Epidermal Growth Factor Receptor Can Counteract the Inhibition of Natural Killer Cell Function Exerted by Colorectal Tumor-Associated Fibroblasts.Frontiers in immunology · 2018Article
- How to Hit Mesenchymal Stromal Cells and Make the Tumor Microenvironment Immunostimulant Rather Than Immunosuppressive.Frontiers in immunology · 2018Review
- PDGF signaling pathway in hepatic fibrosis pathogenesis and therapeutics (Review).Molecular medicine reports · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously demonstrated that non-toxic doses of Celecoxib induced the immediate phosphorylation of Erk1-2 in colon tumor associated fibroblasts (TAFs), increasing their responsiveness to epidermal growth factor (EGF). We have now identified two concomitant mechanisms explaining the EGF-Celecoxib cooperation. We found that a 24-48h Celecoxib priming increased EGF receptor (EGFR) mRNA and protein levels in colon TAFs, promoting EGF binding and internalization. Celecoxib-primed TAFs showed a reduced EGFR degradation after EGF challenge. This delay corresponded to a deferred dissociation of EEA1 from EGFR positive endosomes and the accumulation of Rab7, pro Cathepsin-D and SQSTM1/p62, suggesting a shared bottleneck in the pathways of late-endosomes/autophagosomes maturation. Celecoxib modulated the levels of target proteins similarly to the inhibitors of endosome/lysosome acidification Bafilomycin-A1 and NH(4)Cl. Cytoplasmic vesicles fractionation showed a reduced maturation of Cathepsin-D in late endosomes and an increased content of EGFR and Rab7 in lysosomes of Celecoxib-treated TAFs.Our data indicate a double mechanism mediating the increased response to EGF of colon TAFs treated with Celecoxib. While EGFR overexpression could be targeted using anti EGFR drugs, the effects on endosome trafficking and protein turnover represents a more elusive target and should be taken into account for any long-term therapy with Celecoxib.
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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.