Abstract
Small extracellular vesicles (small EVs) are commonly released by all cells, and are found in all body fluids. They are implicated in cell to cell short- and long-distance communication through the transfer of genetic material and proteins, as well as interactions between target cell membrane receptors and ligands anchored on small EV membrane. Beyond their canonical functions in healthy tissues, small EVs are strategically used by tumors to communicate with the cellular microenvironment and to establish a proper niche which would ultimately allow cancer cell proliferation, escape from the immune surveillance, and metastasis formation. In this review, we highlight the effects of hematological malignancy-derived small EVs on immune and stromal cells in the tumor microenvironment.
Highlights
Our review follows the “Minimal information for studies of extracellular vesicles 2018(MISEV2018)” updated guidelines [1]
This effect is highly decreased if the Acute Promyelocytic Leukemia (APML) cells are treated with all-trans retinoic acid (ATRA), a PML-RARα antagonist typically used in the clinic [219]
Through the multiple strategies and tools deployed by cancer cells to gain proliferative and survival advantages, small extracellular vesicles are one of the most concealed
Summary
Our review follows the “Minimal information for studies of extracellular vesicles 2018. Considered a physiological phenomenon to remove cellular waste, today, small EVs are considered to be a sophisticated way for cells to communicate with the surrounding microenvironment [7,11]. Their molecular content is strictly dependent on the cell of origin [10]. It was shown that tumor-derived small EVs (TEVs) carry a cargo of molecules that is different from the small EVs released by the healthy counterpart [10]. Cells 2019, 8, 511 that tumor cells release specific small EVs containing an unique molecular fingerprint which is used by tumors to increase proliferation [12], metastasis formation [12,13] and immune escape [14], effectively reshaping the healthy microenvironment in favor of a pro-tumorigenic one
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