ArticleBMC cancer2019
Endothelial cell-derived nidogen-1 inhibits migration of SK-BR-3 breast cancer cells.
Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Nidogen-1 suppresses cell proliferation, migration, and glycolysis via integrin β1-mediated HIF-1α downregulation in triple-negative breast cancer.Scientific reports · 2025Article
- Unveiling the Dichotomy of Urinary Proteins: Diagnostic Insights into Breast and Prostate Cancer and Their Roles.Proteomes · 2023Review
- The dynamic tumor-stromal crosstalk: implications of 'stromal-hot' tumors in the process of epithelial-mesenchymal transition in breast cancer.Molecular biology reports · 2023Review
- Review
- Clinical features and lipid metabolism genes as potential biomarkers in advanced lung cancer.BMC cancer · 2023Article
- Identification of novel urine proteomic biomarkers for high stamina in high-altitude adaptation.Frontiers in physiology · 2023Article
- Abnormal promoter DNA hypermethylation of the integrin, nidogen, and dystroglycan genes in breast cancer.Scientific reports · 2021Article
- Nidogen 1 regulates proliferation and migration/invasion in murine claudin-low mammary tumor cells.Oncology letters · 2021Article
- Transcriptome Analysis of Effects of Folic Acid Supplement on Gene Expression in Liver of Broiler Chickens.Frontiers in veterinary science · 2021Article
- Nidogen 1-Enriched Extracellular Vesicles Facilitate Extrahepatic Metastasis of Liver Cancer by Activating Pulmonary Fibroblasts to Secrete Tumor Necrosis Factor Receptor 1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- ECM1 secreted by HER2-overexpressing breast cancer cells promotes formation of a vascular niche accelerating cancer cell migration and invasion.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Proteomic Technology "Lens" for Epithelial-Mesenchymal Transition Process Identification in Oncology.Analytical cellular pathology (Amsterdam) · 2019Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundThe tumour microenvironment is a critical regulator of malignant cancer progression. While endothelial cells have been widely studied in the context of tumour angiogenesis, their role as modulators of cancer cell invasion and migration is poorly understood.
methodsWe have investigated the influence of endothelial cells on the invasive and migratory behaviour of human cancer cells in vitro.
resultsUpon exposure to culture supernatants of endothelial cells, distinct cancer cells, such as SK-BR-3 cells, showed significantly increased invasion and cell migration concomitant with changes in cell morphology and gene expression reminiscent of an epithelial-mesenchymal transition (EMT). Interestingly, the pro-migratory effect on SK-BR-3 cells was significantly enhanced by supernatants obtained from subconfluent, proliferative endothelial cells rather than from confluent, quiescent endothelial cells. Systematically comparing the supernatants of subconfluent and confluent endothelial cells by quantitative MS proteomics revealed eight candidate proteins that were secreted at significantly higher levels by confluent endothelial cells representing potential inhibitors of cancer cell migration. Among these proteins, nidogen-1 was exclusively expressed in confluent endothelial cells and was found to be necessary and sufficient for the inhibition of SK-BR-3 cell migration. Indeed, SK-BR-3 cells exposed to nidogen-1-depleted endothelial supernatants showed increased promigratory STAT3 phosphorylation along with increased cell migration. This reflects the situation of enhanced SK-BR-3 migration upon stimulation with conditioned medium from subconfluent endothelial cells with inherent absence of nidogen-1 expression.
conclusionThe identification of nidogen-1 as an endothelial-derived inhibitor of migration of distinct cancer cell types reveals a novel mechanism of endothelial control over cancer progression.
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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.