Abstract
The tumour microenvironment (TME) plays a crucial role in the regulation of cell survival and growth by providing inhibitory or stimulatory signals. Extracellular vesicles (EV) represent one of the most relevant cell-to-cell communication mechanism among cells within the TME. Moreover, EV contribute to the crosstalk among cancerous, immune, endothelial, and stromal cells to establish TME diversity. EV contain proteins, mRNAs and miRNAs, which can be locally delivered in the TME and/or transferred to remote sites to dictate tumour behaviour. EV in the TME impact on cancer cell proliferation, invasion, metastasis, immune-escape, pre-metastatic niche formation and the stimulation of angiogenesis. Moreover, EV can boost or inhibit tumours depending on the TME conditions and their cell of origin. Therefore, to move towards the identification of new targets and the development of a novel generation of EV-based targeting approaches to gain insight into EV mechanism of action in the TME would be of particular relevance. The aim here is to provide an overview of the current knowledge of EV released from different TME cellular components and their role in driving TME diversity. Moreover, recent proposed engineering approaches to targeting cells in the TME via EV are discussed.
Highlights
Extracellular vesicles (EV) include 100–5000 nm vesicles released by almost all cell types.Exosomes are a subclass of extracellular vesicles ranging from 40 to 150 nm derived from multivesicular bodies, and are distinct for their biogenesis from ectosomes and pre-apoptotic vesicles, as the latter originate from the budding of the cell plasma membrane [1]
EV are detected in the tumour microenvironment (TME), and emerging evidence suggests that they play a role in facilitating tumourigenesis by regulating different processes, including tumour growth, angiogenesis, immunity, and metastasis formation
The enrichment of miRNA-1228 in cancer associated fibroblasts (CAF), in their secreted EV and in recipient tumour cells has been linked to the downregulation of the endogenous suppressor of cancer cell invasion (SCAI), a novel and highly conserved protein involved in invasiveness of osteosarcoma cells [71]
Summary
Extracellular vesicles (EV) include 100–5000 nm vesicles released by almost all cell types. 21, in canJ. be 2020, found the TME, which include dendritic cells (DC), B-lymphocytes, T-lymphocytes, natural killer (NK) cells, and macrophages [9,10] All these cells shed EV, and contribute to TME diversity [11] (Figure 1). The tumour microenvironment (TME) contains cancer cells, displaying different phenotypes heterogeneity of circulating EV, they have been considered to be a fingerprint of the tumour. The aim of this review is to give an overview natural killer (NK) cells, and macrophages [9,10] All these cells shed EV, and contribute to TME of the current knowledge on EV functional diversity in the tumour setting, with particular emphasis diversity [11] (Figure 1).
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