Abstract
Extracellular vesicles (EVs) are important mediators of intercellular communication in cancer and in normal tissues. EVs transfer biologically active molecules from the cell of origin to recipient cells. This review summarizes the studies on EVs derived from renal cell carcinoma and from a subpopulation of CD105-positive renal cancer stem cells. While EVs from renal cell carcinoma show mild biological activity, EVs from renal cancer stem cells enhance tumor angiogenesis and metastasis formation. The effect is probably due to the transfer of proangiogenic RNA cargo to endothelial cells, which acquire an activated angiogenic phenotype. In vivo, treatment with EVs favors the formation of a premetastatic niche in the lungs. Moreover, EVs derived from renal cancer stem cells modify gene expression in mesenchymal stromal cells, enhancing the expression of genes involved in matrix remodeling, cell migration, and tumor growth. Mesenchymal stromal cells preconditioned with tumor EVs and then coinjected in vivo with renal cancer cells support tumor growth and vessel formation. Finally, tumor EVs promote tumor immune escape by inhibiting the differentiation process of dendritic cells and the activation of T cells. Thus, tumor-derived EVs act on the microenvironment favoring tumor aggressiveness, may contribute to angiogenesis through both direct and indirect mechanisms and are involved in tumor immune escape.
Highlights
Cancer cells, as well as all other cells, are capable of releasing extracellular vesicles (EVs) into the extracellular space
An enhanced expression of VEGFR1 protein and VEGF and MMP2 genes in lung endothelial cells, and MMP9 gene in lung tissue was observed after treatment with Renal CSCs (rCSCs)-EVs, but not with EVs derived from non-stem renal cancer cells
The authors evaluated the ability of rCSC-EVs and EVs derived from non-stem renal cancer cells to inhibit DC differentiation by culturing monocytes in the presence of EVs. rCSC-EVs interfered with the phenotype of monocyte-derived cells, with a reduced expression of activation markers CD83 and CD40, costimulatory molecules CD80 and CD86, antigen-presenting molecule HLA-DR, and adhesion molecules involved in T-cell contact
Summary
Chiara Gai[1], Margherita A. Pomatto[1], Cristina Grange[1], Maria Chiara Deregibus[2] and Giovanni Camussi[1,2]
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