Microenvironmental interactions between endothelial and lymphoma cells: a role for the canonical WNT pathway in Hodgkin lymphoma
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
27535218
DOI
10.1038/leu.2016.232
PII: leu2016232
Knihovny.cz E-zdroje
- MeSH
- beta-katenin genetika metabolismus MeSH
- buněčná adheze genetika MeSH
- buněčné linie MeSH
- chemokin CCL19 metabolismus MeSH
- chemotaxe genetika imunologie MeSH
- endoteliální buňky metabolismus MeSH
- Hodgkinova nemoc genetika imunologie metabolismus patologie MeSH
- lidé MeSH
- mezibuněčná komunikace * MeSH
- nádorové mikroprostředí * genetika imunologie MeSH
- patologická angiogeneze MeSH
- pohyb buněk genetika MeSH
- signální dráha Wnt * MeSH
- transkripční faktor LEF-1 genetika metabolismus MeSH
- vaskulární endoteliální růstový faktor A metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- beta-katenin MeSH
- chemokin CCL19 MeSH
- transkripční faktor LEF-1 MeSH
- vaskulární endoteliální růstový faktor A MeSH
The interaction between vascular endothelial cells (ECs) and cancer cells is of vital importance to understand tumor dissemination. A paradigmatic cancer to study cell-cell interactions is classical Hodgkin Lymphoma (cHL) owing to its complex microenvironment. The role of the interplay between cHL and ECs remains poorly understood. Here we identify canonical WNT pathway activity as important for the mutual interactions between cHL cells and ECs. We demonstrate that local canonical WNT signaling activates cHL cell chemotaxis toward ECs, adhesion to EC layers and cell invasion using not only the Wnt-inhibitor Dickkopf, tankyrases and casein kinase 1 inhibitors but also knockdown of the lymphocyte enhancer binding-factor 1 (LEF-1) and β-catenin in cHL cells. Furthermore, LEF-1- and β-catenin-regulated cHL secretome promoted EC migration, sprouting and vascular tube formation involving vascular endothelial growth factor A (VEGF-A). Importantly, high VEGFA expression is associated with a worse overall survival of cHL patients. These findings strongly support the concept that WNTs might function as a regulator of lymphoma dissemination by affecting cHL cell chemotaxis and promoting EC behavior and thus angiogenesis through paracrine interactions.
Central European Institute of Technology Masaryk University Brno Czech Republic
Department of Chemical Biology Helmholtz Centre for Infection Research HZI Braunschweig Germany
Faculty of Science Institute of Experimental Biology Masaryk University Brno Czech Republic
Institute of Biostatistics and Analyses Masaryk University Brno Czech Republic
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