ArticleScientific reports2017
VE-Cadherin Disassembly and Cell Contractility in the Endothelium are Necessary for Barrier Disruption Induced by Tumor Cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 51 citations in OpenAlex.
- IFN-γ drives inflammatory bowel disease pathogenesis through VE-cadherin-directed vascular barrier disruption.The Journal of clinical investigation · 2019Trial
- Lyophilized Synthetic Platelets: In Vitro Characterization and In Vivo Evaluation in Mouse Thrombocytopenia Model.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Protein Kinase C-Delta (PKCδ) inhibition stabilizes endothelium and suppresses triple-negative breast cancer (TNBC) intravasation in a microfluidic hypoxic tumor model.Bioengineering & translational medicine · 2026Article
- Unveiling the intricate dynamics of the interplay between triple-negative breast cancer cells and the blood-brain barrier endothelium.Acta neuropathologica communications · 2025Article
- Cancer cells impact the microrheology of endothelial cells during physical contact or through paracrine signalling.Scientific reports · 2025Article
- Molecular Findings Before Vision Loss in the Streptozotocin-Induced Rat Model of Diabetic Retinopathy.Current issues in molecular biology · 2025Review
- Angiogenesis-Enabled Human Ovarian Tumor Microenvironment-Chip Evaluates Pathophysiology of Platelets in Microcirculation.Advanced healthcare materials · 2024Article
- Signaling crosstalk between tumor endothelial cells and immune cells in the microenvironment of solid tumors.Frontiers in cell and developmental biology · 2024Review
- Innovative and potential treatments for fungal central nervous system infections.Current opinion in microbiology · 2023Review
- Long Non-Coding RNAs as Novel Targets for Phytochemicals to Cease Cancer Metastasis.Molecules (Basel, Switzerland) · 2023Review
- Transforming growth factor-β-induced secretion of extracellular vesicles from oral cancer cells evokes endothelial barrier instability via endothelial-mesenchymal transition.Inflammation and regeneration · 2022Article
- The biophysics of cancer: emerging insights from micro- and nanoscale tools.Advanced nanobiomed research · 2022Article
- Comparative Analysis of Blood-Derived Endothelial Cells for Designing Next-Generation Personalized Organ-on-Chips.Journal of the American Heart Association · 2021Article
- The role of redox system in metastasis formation.Angiogenesis · 2021Review
- A High-Content Screen Identifies Drugs That Restrict Tumor Cell Extravasation across the Endothelial Barrier.Cancer research · 2021Article
- Minimal Residual Disease, Metastasis and Immunity.Biomolecules · 2021Review
- Analysis of Differentially Expressed Genes in Endothelial Cells Following Tumor Cell Adhesion, and the Role of PRKAA2 and miR-124-3p.Frontiers in cell and developmental biology · 2021Article
- Rho GTPase signalling networks in cancer cell transendothelial migration.Vascular biology (Bristol, England) · 2021Review
- OvCa-Chip microsystem recreates vascular endothelium-mediated platelet extravasation in ovarian cancer.Blood advances · 2020Article
- Podosome formation impairs endothelial barrier function by sequestering zonula occludens proteins.Journal of cellular physiology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During metastasis, breakdown of the endothelial barrier is critical for tumor cell extravasation through blood vessel walls and is mediated by a combination of tumor secreted soluble factors and receptor-ligand interactions. However, a complete mechanism governing tumor cell transendothelial migration remains unclear. Here, we investigate the roles of tumor-associated signals in regulating endothelial cell contractility and adherens junction disassembly leading to endothelial barrier breakdown. We show that Src mediates VE-cadherin disassembly in response to metastatic melanoma cells. Through the use of pharmacological inhibitors of cytoskeletal contractility we find that endothelial cell contractility is responsive to interactions with metastatic cancer cells and that reducing endothelial cell contractility abrogates migration of melanoma cells across endothelial monolayers. Furthermore, we find that a combination of tumor secreted soluble factors and receptor-ligand interactions mediate activation of Src within endothelial cells that is necessary for phosphorylation of VE-cadherin and for breakdown of the endothelial barrier. Together, these results provide insight into how tumor cell signals act in concert to modulate cytoskeletal contractility and adherens junctions disassembly during extravasation and may aid in identification of therapeutic targets to block metastasis.
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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.