ArticleVascular pharmacology2017
Colon cancer-derived myofibroblasts increase endothelial cell migration by glucocorticoid-sensitive secretion of a pro-migratory factor.
Article in Vascular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 25 citations in OpenAlex.
- Cellular crosstalk of fibroblast-myofibroblast transition in intestinal homeostasis and disease.Biomarker research · 2026Review
- Contribution of tumor microenvironment (TME) to tumor apoptosis, angiogenesis, metastasis, and drug resistance.Medical oncology (Northwood, London, England) · 2025Review
- Radiosynthesis andFrontiers in oncology · 2024Article
- Energy level as a theranostic factor for successful therapy of tissue injuries with polyphosphate: the triad metabolic energy - mechanical energy - heat.Theranostics · 2024Article
- Cytokines: Can Cancer Get the Message?Cancers · 2022Review
- Angiopoietin-like Proteins in Colorectal Cancer-A Literature Review.International journal of molecular sciences · 2021Review
- Angiogenin regulates PKD activation and COX-2 expression induced by TNF-α and bradykinin in the colonic myofibroblast.Biochemical and biophysical research communications · 2020Article
- In search of definitions: Cancer-associated fibroblasts and their markers.International journal of cancer · 2020Review
- Cellular and Extracellular Components in Tumor Microenvironment and Their Application in Early Diagnosis of Cancers.Analytical cellular pathology (Amsterdam) · 2020Review
- Breast Cancer Resistance Protein (BCRP/Cells · 2019Article
- Exploiting vulnerabilities of cancer by targeting nuclear receptors of stromal cells in tumor microenvironment.Molecular cancer · 2019Review
- Calotropin regulates the apoptosis of non‑small cell cancer by regulating the cytotoxic T‑lymphocyte associated antigen 4‑mediated TGF‑β/ERK signaling pathway.Molecular medicine reports · 2018Article
- Species-specific regulation of angiogenesis by glucocorticoids reveals contrasting effects on inflammatory and angiogenic pathways.PloS one · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Angiogenesis is important in cancer progression and can be influenced by tumor-associated myofibroblasts. We addressed the hypothesis that glucocorticoids indirectly affect angiogenesis by altering the release of pro-angiogenic factors from colon cancer-derived myofibroblasts. Our study shows that glucocorticoids reduced prostanoids, urokinase-type plasminogen activator (uPA) and angiopoietin-like protein-2 (ANGPTL2) levels, but increased angiogenin (ANG) in supernatant from human CT5.3hTERT colon cancer-derived myofibroblasts. Conditioned medium from solvent- (CMS) and dexamethasone (Dex)-treated (CMD) myofibroblasts increased human umbilical vein endothelial cell (HUVEC) proliferation, but did not affect expression of pro-angiogenic factors or tube-like structure formation (by HUVECs or human aortic ECs). In a HUVEC scratch assay CMS-induced acceleration of wound healing was blunted by CMD treatment. Moreover, CMS-induced neovessel growth in mouse aortic rings ex vivo was also blunted using CMD. The latter effect could be ascribed to both Dex-driven reduction of secreted factors and potential residual Dex present in CMD (indicated using a dexamethasone-spiked CMS control). A similar control in the scratch assay, however, revealed that altered levels of factors in the CMD, and not potential residual Dex, were responsible for decreased wound closure. In conclusion, our results suggest that glucocorticoids indirectly alter endothelial cell function during tumor development in vivo.
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