Abstract

Extracellular vesicles (EVs) are membrane vesicles, which are secreted by a variety of cells that have a relevant role in intercellular communication. EVs derived from various cell types exert different effects on target cells. Mesenchymal stromal cells (MSCs) are stem cells that are ubiquitously present in different tissues of the human body, and MSC-derived EVs take part in a wide range of biological processes. Of particular relevance is the effect of MSCs on tumor growth and progression. MSCs have opposing effects on tumor growth, being able either to favor angiogenesis and tumor initiation, or to inhibit progression of established tumors, according to the conditions. Different studies have reported that EVs from MSCs may exert either an anti- or a pro-tumor growth effect depending on tumor type and stage of development. In this review, we will discuss the data presented in the literature on EV-mediated interactions between MSCs and tumors.

Highlights

  • Mesenchymal stromal cells (MSCs) are multipotent cells that reside in various tissues, and possess the capacity to differentiate into different mesodermal lineages [1,2,3,4,5,6,7,8]

  • MSCs isolated from different tissues, such as human adipose tissue [24], breast [25], and palatine tonsils [26], have been shown to have the capacity to interfere with cancer cell proliferation, blocking tumor cell cycle in G0/G1 phases

  • In the contest of cancer, Extracellular vesicles (EVs) derived from MSCs have been shown to mimic most of the beneficial and detrimental effects of the cells of origin

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Summary

INTRODUCTION

Mesenchymal stromal cells (MSCs) are multipotent cells that reside in various tissues, and possess the capacity to differentiate into different mesodermal lineages [1,2,3,4,5,6,7,8]. Extracellular vesicles derived from murine MSCs were shown to significantly down-regulate the expression of vascular endothelial growth factor (VEGF) in breast cancer cells, causing an inhibition of angiogenesis both in vitro and in vivo [53]. The same group that demonstrated the anti-tumor activity of hWJMSC-EVs in bladder cancer recently reported that the same EVs can promote growth and aggressiveness of a renal carcinoma cell line (786-0), both in vitro and in vivo [56]. In this context, after 48 h of incubation, EVs facilitated the cell cycle progression from G0/G1 to S phase. Pre-treatment of EVs with RNase abrogated both the in vitro

Hepatoma Lymphoblast Glioblastoma
CONCLUSIONS
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