ArticlePloS one2014
VE-cadherin-independent cancer cell incorporation into the vascular endothelium precedes transmigration.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 31 citations in OpenAlex.
- Substrate stiffness and cellular microenvironment regulate cell and junction mechanics in iPSC-derived brain microvascular endothelial cells.bioRxiv : the preprint server for biology · 2026Article
- Aquaporin 5 transfer via MDA-MB-231 cell extracellular vesicles increases recipient endothelial cell invasion.Biochemical and biophysical research communications · 2025Article
- Unveiling the intricate dynamics of the interplay between triple-negative breast cancer cells and the blood-brain barrier endothelium.Acta neuropathologica communications · 2025Article
- Increased basal fibronectin is sufficient to promote excess endothelial cell matrix assembly causing localized barrier dysfunction.Molecular biology of the cell · 2024Article
- Mechanisms of triple-negative breast cancer extravasation: Impact of the physical environment and endothelial glycocalyx.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- Review
- CGX, a standardized herbal syrup, inhibits colon-liver metastasis by regulating the hepatic microenvironments in a splenic injection mouse model.Frontiers in pharmacology · 2022Article
- Morphological Phenotyping of Organotropic Brain- and Bone-Seeking Triple Negative Metastatic Breast Tumor Cells.Frontiers in cell and developmental biology · 2022Article
- The Influence of VE-Cadherin on Adhesion and Incorporation of Breast Cancer Cells into Vascular Endothelium.International journal of molecular sciences · 2021Article
- Cutaneous melanoma dissemination is dependent on the malignant cell properties and factors of intercellular crosstalk in the cancer microenvironment (Review).International journal of oncology · 2020Review
- Quantitatively relating brain endothelial cell-cell junction phenotype to global and local barrier properties under varied culture conditions via the Junction Analyzer Program.Fluids and barriers of the CNS · 2020Article
- Review
- Mechanosensing of Mechanical Confinement by Mesenchymal-Like Cells.Frontiers in physiology · 2020Review
- Tumor Cell Mechanosensing During Incorporation into the Brain Microvascular Endothelium.Cellular and molecular bioengineering · 2019Article
- Paracellular and transcellular migration of metastatic cells through the cerebral endothelium.Journal of cellular and molecular medicine · 2019Article
- Ultrathin Dual-Scale Nano- and Microporous Membranes for Vascular Transmigration Models.Small (Weinheim an der Bergstrasse, Germany) · 2019Article
- Foe or friend? Janus-faces of the neurovascular unit in the formation of brain metastases.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Review
- Extracellular matrix stiffness and cell contractility control RNA localization to promote cell migration.Nature communications · 2017Article
- A microfluidic platform for modeling metastatic cancer cell matrix invasion.Biofabrication · 2017Article
- VE-Cadherin Disassembly and Cell Contractility in the Endothelium are Necessary for Barrier Disruption Induced by Tumor Cells.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Metastasis is accountable for 90% of cancer deaths. During metastasis, tumor cells break away from the primary tumor, enter the blood and the lymph vessels, and use them as highways to travel to distant sites in the body to form secondary tumors. Cancer cell migration through the endothelium and into the basement membrane represents a critical step in the metastatic cascade, yet it is not well understood. This process is well characterized for immune cells that routinely transmigrate through the endothelium to sites of infection, inflammation, or injury. Previous studies with leukocytes have demonstrated that this step depends heavily on the activation status of the endothelium and subendothelial substrate stiffness. Here, we used a previously established in vitro model of the endothelium and live cell imaging, in order to observe cancer cell transmigration and compare this process to leukocytes. Interestingly, cancer cell transmigration includes an additional step, which we term 'incorporation', into the endothelial cell (EC) monolayer. During this phase, cancer cells physically displace ECs, leading to the dislocation of EC VE-cadherin away from EC junctions bordering cancer cells, and spread into the monolayer. In some cases, ECs completely detach from the matrix. Furthermore, cancer cell incorporation occurs independently of the activation status and the subendothelial substrate stiffness for breast cancer and melanoma cells, a notable difference from the process by which leukocytes transmigrate. Meanwhile, pancreatic cancer cell incorporation was dependent on the activation status of the endothelium and changed on very stiff subendothelial substrates. Collectively, our results provide mechanistic insights into tumor cell extravasation and demonstrate that incorporation is one of the earliest steps.
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