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@article{1380329,
author = {Hauselmann, Irina and Roblek, Marko and Protsyuk, Darya and Huck, Volker and Knopfová, Lucia and Grassle, Sandra and Bauer, Alexander T. and Schneider, Stefan W. and Borsig, Lubor},
article_location = {USA},
article_number = {18},
doi = {http://dx.doi.org/10.1158/0008-5472.CAN-16-0784},
keywords = {VASCULAR ENDOTHELIUM; PROTEIN-KINASE; CANCER-CELLS; TRANSENDOTHELIAL MIGRATION; ADHESION MOLECULES; LIVER METASTASIS; P-SELECTIN; EXPRESSION; RECRUITMENT; GROWTH},
language = {eng},
issn = {0008-5472},
journal = {Cancer Research},
title = {Monocyte Induction of E-Selectin-Mediated Endothelial Activation Releases VE-Cadherin Junctions to Promote Tumor Cell Extravasation in the Metastasis Cascade},
volume = {76},
year = {2016}
}
TY - JOUR
ID - 1380329
AU - Hauselmann, Irina - Roblek, Marko - Protsyuk, Darya - Huck, Volker - Knopfová, Lucia - Grassle, Sandra - Bauer, Alexander T. - Schneider, Stefan W. - Borsig, Lubor
PY - 2016
TI - Monocyte Induction of E-Selectin-Mediated Endothelial Activation Releases VE-Cadherin Junctions to Promote Tumor Cell Extravasation in the Metastasis Cascade
JF - Cancer Research
VL - 76
IS - 18
SP - 5302-5312
EP - 5302-5312
PB - American Association for Cancer Research
SN - 00085472
KW - VASCULAR ENDOTHELIUM
KW - PROTEIN-KINASE
KW - CANCER-CELLS
KW - TRANSENDOTHELIAL MIGRATION
KW - ADHESION MOLECULES
KW - LIVER METASTASIS
KW - P-SELECTIN
KW - EXPRESSION
KW - RECRUITMENT
KW - GROWTH
N2 - 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 transendothelial 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. (C) 2016 AACR.
ER -
HAUSELMANN, Irina, Marko ROBLEK, Darya PROTSYUK, Volker HUCK, Lucia KNOPFOVÁ, Sandra GRASSLE, Alexander T. BAUER, Stefan W. SCHNEIDER and Lubor BORSIG. Monocyte Induction of E-Selectin-Mediated Endothelial Activation Releases VE-Cadherin Junctions to Promote Tumor Cell Extravasation in the Metastasis Cascade. \textit{Cancer Research}. USA: American Association for Cancer Research, 2016, vol.~76, No~18, p.~5302-5312. ISSN~0008-5472. Available from: https://dx.doi.org/10.1158/0008-5472.CAN-16-0784.
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