Abstract
Extracellular vesicles (EVs) are nanosized particles released by numerous kinds of cells, which are now increasingly considered as essential vehicles of cell-to-cell communication and biomarkers in disease diagnosis and treatment. They contain a variety of biomolecular components, including lipids, proteins and nucleic acids. These functional molecules can be transmitted between tumor cells and other stromal cells such as endothelial cells, fibroblasts and immune cells utilizing EVs. As a result, tumor-derived EVs can deliver molecules to remodel the tumor microenvironment, thereby influencing cancer progression. On the one hand, tumor-derived EVs reprogram functions of endothelial cells, promote cancer-associated fibroblasts transformation, induce resistance to therapy and inhibit the immune response to form a pro-tumorigenic environment. On the other hand, tumor-derived EVs stimulate the immune response to create an anti-tumoral environment. This article focuses on presenting a comprehensive and critical overview of the potential role of tumor-derived EVs-mediated communication in the tumor microenvironment.
Highlights
Extracellular vesicles (EVs), including exosomes and ectosomes, are nanoscale particles released by most types of cells (Théry et al, 2018)
EVs isolated from human vascular endothelial cells contain some cardioprotective proteins, which contribute to promoting human myocardium survival after ischemia-reperfusion injury (Yadid et al, 2020)
EVs derived from breast cancer enhance the ability of cancer-associated fibroblasts (CAFs) in response to different metabolic environment by activating MYC signaling pathway in stromal cells resulting in rapid tumor growth (Yan et al, 2018)
Summary
Extracellular vesicles (EVs), including exosomes and ectosomes, are nanoscale particles released by most types of cells (Théry et al, 2018). Tumor-derived EVs can regulate cancer-associated fibroblasts (CAFs) transformation. EVs derived from breast cancer enhance the ability of CAFs in response to different metabolic environment by activating MYC signaling pathway in stromal cells resulting in rapid tumor growth (Yan et al, 2018).
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