Abstract
Extracellular vesicles (EVs) are considered to be a novel complex mechanism of cell communication within the tumor microenvironment. EVs may act as vehicles for transcription factors and nucleic acids inducing epigenetic changes in recipient cells. Since tumor EVs may be present in patient biological fluids, it is important to investigate their function and molecular mechanisms of action. It has been shown that tumor cells release EVs, which are capable of regulating cell apoptosis, proliferation, invasion, and epithelial–mesenchymal transition, as well as to suppress activity of immune cells, to enhance angiogenesis, and to prepare a favorable microenvironment for metastasis. On the other hand, EVs derived from stromal cells, such as mesenchymal stem cells (MSCs), may influence the phenotype of tumor cells through reciprocal cross talk greatly influenced by the transcription factors and nucleic acids they carry. In particular, non-coding RNAs (ncRNAs), including microRNAs and long ncRNAs, have recently been identified as the main candidates for the phenotypic changes induced in the recipient cells by EVs. ncRNAs, which are important regulators of mRNA and protein expression, can function either as tumor suppressors or as oncogenes, depending on their targets. Herein, we have attempted to revise actual evidence reported in the literature on the role of EVs in tumor biology with particular regard to the cross talk of ncRNAs between cancer cells and MSCs.
Highlights
Extracellular vesicles (EVs) have recently been identified to be instrumental in intercellular communication through the exchange of biologically active molecules, in particular, non-coding RNAs that can modulate gene expression locally and systemically [1,2,3]
We mainly focus on the role of non-coding RNAs (ncRNAs) carried by tumoral extracellular vesicles (T-EVs) and by mesenchymal stem cells (MSCs)-derived EVs (MSC-EVs) in modification of tumor microenvironment with particular regard to the interaction between cancer cells and MSCs
Several studies indicate that cancer stem cells (CSCs) release EVs that may contribute to tumor initiation and progression by stimulation of cell proliferation, invasion, angiogenesis, and metastasis formation, as well as by the promotion of tumor immune escape [29, 140,141,142,143]
Summary
Extracellular vesicles (EVs) have recently been identified to be instrumental in intercellular communication through the exchange of biologically active molecules, in particular, non-coding RNAs (ncRNA) that can modulate gene expression locally and systemically [1,2,3]. Non-coding RNAs are usually divided into two major groups according to their length These include small ncRNAs (below 200 nt) defined as microRNAs (miRNAs), and the long ncRNAs (lncRNAs; above 200 nt). Tumors contain a heterogeneous population of cells, including mesenchymal stem cells (MSCs), endothelial cells, cancer-associated fibroblasts, immune inflammatory cells, and cancer stem cells (CSCs) Communication between these cells and cells present in the normal surrounding tissue helps tumor-initiating cells to survive, proliferate, invade, and establish metastasis [17,18,19]. We mainly focus on the role of ncRNAs carried by T-EVs and by MSC-derived EVs (MSC-EVs) in modification of tumor microenvironment with particular regard to the interaction between cancer cells and MSCs
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