Open AccessEndothelial extracellular vesicles promote tumour growth by tumour‐associated macrophage reprogramming
Author(s) -
Njock MakonSébastien,
O'Grady Tina,
Nivelles Olivier,
Lion Michelle,
Jacques Sophie,
Cambier Maureen,
Herkenne Stephanie,
Muller Florian,
Christian Aurélie,
Remacle Claire,
Guiot Julien,
Rahmouni Souad,
Dequiedt Franck,
Struman Ingrid
Publication year - 2022
Publication title -
journal of extracellular vesicles
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.94
H-Index - 68
ISSN - 2001-3078
DOI - 10.1002/jev2.12228
Subject(s) - microrna , microvesicles , angiogenesis , biology , macrophage polarization , phenotype , extracellular vesicles , reprogramming , microbiology and biotechnology , macrophage , immune system , extracellular vesicle , cancer research , microvesicle , inflammation , tumor microenvironment , immunology , cell , gene , in vitro , genetics
Tumour‐derived extracellular vesicles (EVs) participate in tumour progression by deregulating various physiological processes including angiogenesis and inflammation. Here we report that EVs released by endothelial cells in a mammary tumour environment participate in the recruitment of macrophages within the tumour, leading to an immunomodulatory phenotype permissive for tumour growth. Using RNA‐Seq approaches, we identified several microRNAs (miRNAs) found in endothelial EVs sharing common targets involved in the regulation of the immune system. To further study the impact of these miRNAs in a mouse tumour model, we focused on three miRNAs that are conserved between humans and mouse, that is, miR‐142‐5p, miR‐183‐5p and miR‐222‐3p. These miRNAs are released from endothelial cells in a tumour microenvironment and are transferred via EVs to macrophages. In mouse mammary tumour models, treatment with EVs enriched in these miRNAs leads to a polarization of macrophages toward an M2‐like phenotype, which in turn promotes tumour growth.