ArticleAmerican journal of physiology. Cell physiology2010
p38 MAP kinase is necessary for melanoma-mediated regulation of VE-cadherin disassembly.
Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 33 citations in OpenAlex.
- Thrombin-Activated Platelets Protect Vascular Endothelium against Tumor Cell Extravasation by Targeting Endothelial VCAM-1.International journal of molecular sciences · 2022Article
- Angiotensin II Induces Cardiac Edema and Hypertrophic Remodeling through Lymphatic-Dependent Mechanisms.Oxidative medicine and cellular longevity · 2022Article
- Heat shock protein 27 activity is linked to endothelial barrier recovery after proinflammatory GPCR-induced disruption.Science signaling · 2021Article
- Caspase-8 modulates physiological and pathological angiogenesis during retina development.The Journal of clinical investigation · 2019Article
- Prolyl Hydroxylase Domain-2 Protein Regulates Lipopolysaccharide-Induced Vascular Inflammation.The American journal of pathology · 2019Article
- Quinic Acid-Conjugated Nanoparticles Enhance Drug Delivery to Solid Tumors via Interactions with Endothelial Selectins.Small (Weinheim an der Bergstrasse, Germany) · 2018Article
- VE-Cadherin Disassembly and Cell Contractility in the Endothelium are Necessary for Barrier Disruption Induced by Tumor Cells.Scientific reports · 2017Article
- Thrombomodulin blocks calcineurin inhibitor-induced vascular permeability via inhibition of Src/VE-cadherin axis.Bone marrow transplantation · 2017Article
- Mutant B-Raf(V600E) Promotes Melanoma Paracellular Transmigration by Inducing Thrombin-mediated Endothelial Junction Breakdown.The Journal of biological chemistry · 2016Article
- Melanoma upregulates ICAM-1 expression on endothelial cells through engagement of tumor CD44 with endothelial E-selectin and activation of a PKCα-p38-SP-1 pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- CD82/KAI expression prevents IL-8-mediated endothelial gap formation in late-stage melanomas.Oncogene · 2014Article
- Article
- Integrin β4 signaling promotes mammary tumor cell adhesion to brain microvascular endothelium by inducing ErbB2-mediated secretion of VEGF.Annals of biomedical engineering · 2011Article
- Tara up-regulates E-cadherin transcription by binding to the Trio RhoGEF and inhibiting Rac signaling.The Journal of cell biology · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Vascular endothelial (VE)-cadherin is localized to the endothelial borders and the adherens junctions, which are regulated by changes in mitogen-activated protein (MAP) kinases, GTPases, and intracellular calcium. We previously showed that melanoma cells induce VE-cadherin disassembly through contact with human umbilical vein endothelial cells in coculture. However, the exact mechanism by which melanoma cells signal endothelial cells to induce VE-cadherin junction disassembly is not well understood. In this study, VE-cadherin junction disassembly was further examined under fluorescence microscopy. We found that melanoma-induced VE-cadherin junction disassembly and upregulation of p38 MAP kinase in endothelial cells is regulated by both soluble factors from melanomas, particularly interleukin (IL)-8, IL-6, and IL-1beta, and through vascular cell adhesion molecule-1. Neutralizing melanoma-secreted soluble factors reduced endothelial gap formation. Endothelial cells transfected with MAP kinase kinase 6, a direct activator of p38 MAP kinase, increased VE-cadherin-mediated gap formation, facilitating melanoma transendothelial migration. In contrast, endothelial cells transfected with small-interfering RNA against p38 MAP kinase expression largely prevented melanoma transendothelial migration in Boyden chamber experiments. These findings indicate that p38 MAP kinase proteins regulate VE-cadherin junction disassembly, facilitating melanoma migration across endothelial cells.
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