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Monocyte induction of E-selectin-mediated endothelial activation releases VE-cadherin junctions to promote tumor cell extravasation in the metastasis cascade

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F16%3A00065498" target="_blank" >RIV/00159816:_____/16:00065498 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216224:14310/16:00094259

  • Result on the web

    <a href="http://dx.doi.org/10.1158/0008-5472.CAN-16-0784" target="_blank" >http://dx.doi.org/10.1158/0008-5472.CAN-16-0784</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1158/0008-5472.CAN-16-0784" target="_blank" >10.1158/0008-5472.CAN-16-0784</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Monocyte induction of E-selectin-mediated endothelial activation releases VE-cadherin junctions to promote tumor cell extravasation in the metastasis cascade

  • Original language description

    Tumor cells interact with blood constituents and these interactions promote metastasis. Selectins are vascular receptors facilitating interactions of tumor cells with platelets, leukocytes and endothelium but the role of endothelial E-selectin remains unclear. Here we show that E-selectin is a major receptor for monocyte recruitment to tumor cell-activated endothelium. Experimental and spontaneous lung metastasis using murine tumor cells, without E-selectin ligands, were attenuated in E-selectin-deficient mice. Tumor cell-derived CCL2 promoted endothelial activation resulting in enhanced endothelial E-selectin expression. The recruitment of inflammatory monocytes to metastasizing tumor cells was dependent on the local endothelial activation and the presence of E-selectin. Monocytes promoted trans-endothelial migration of tumor cells through the induction of E-selectin-dependent endothelial retractions and a subsequent modulation of tight junctions through dephosphorylation of VE-cadherin. Thus, endothelial E-selectin shapes the tumor microenvironment through the recruitment, adhesion and activation of monocytes that facilitate tumor cell extravasation and thereby metastasis. These findings provide evidence that endothelial E-selectin is a novel factor contributing to endothelial retraction required for efficient lung metastasis.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)

  • CEP classification

    FD - Oncology and haematology

  • OECD FORD branch

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2016

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Cancer Research

  • ISSN

    0008-5472

  • e-ISSN

  • Volume of the periodical

    76

  • Issue of the periodical within the volume

    18

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    11

  • Pages from-to

    5302-5312

  • UT code for WoS article

    000383358300013

  • EID of the result in the Scopus database