Abstract
Exosomes are nanosized vesicles, derived from the endolysosomal compartment of cells and can shuttle diverse biomolecules such as nucleic acids, proteins, lipids, amino acids, and metabolites, which can reflect their origin cells. Delivery of these cargoes to recipient cells enables exosomes to influence diverse cellular functions. As one of the most abundant immune cells in the tumor microenvironment, tumor-associated macrophages (TAMs) are educated by the tumor milieu, which is rich in cancer cells and stroma components, to exert functions such as the promotion of tumor growth, immunosuppression, angiogenesis, and cancer cell dissemination. Herein, we focus on exosomes-mediated intercellular communication between tumor cells and TAM in the tumor microenvironment, which may provide new targets for anti-tumor treatment. In this review, we highlight the most recent studies on the effect of tumor/macrophage-derived exosomes on macrophage/tumor function in different cancer types.
Highlights
The study of extacellular vesicles (EVs) is continuously evolving, they generally divide into two major categories, exosomes (40–160 nm) and ectosomes (50 nm-1 μm in diameter, including microvesicles, microparticles and large vesicles) (Meldolesi, 2018; Kalluri and LeBleu, 2020)
The miR-1246-enriched exosomes derived from TP53 mutants cancer cells are uptaken by macrophages and trigger them to reprogram into a tumor supportive and anti-inflammatory state via TGF-β activation (Cooks et al, 2018), and hypoxic gliomaderived exosomal miR-1246 induces M2 phenotype by targeting TERF2IP to activate the STAT3 signaling pathway and inhibit the NF-κB signaling pathway (Qian et al, 2020), subsequently promoting tumor proliferation, migration and invasion
These results indicate that blocking cancer cellmacrophage communication mediated by exosomes may be a potential strategy for tumor treatment
Summary
The study of extacellular vesicles (EVs) is continuously evolving, they generally divide into two major categories, exosomes (40–160 nm) and ectosomes (50 nm-1 μm in diameter, including microvesicles, microparticles and large vesicles) (Meldolesi, 2018; Kalluri and LeBleu, 2020). OSCC-derived exosomal miR-29a-3p induces M2 polarization in macrophages and directly targets the suppressor of cytokine signaling (SOCS)1/STAT6 signaling to promote tumor growth (Cai et al, 2019).
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