Abstract
Different types of cells, such as endothelial cells, tumor-associated fibroblasts, pericytes, and immune cells, release extracellular vesicles (EVs) in the tumor microenvironment. The components of EVs include proteins, DNA, RNA, and microRNA. One of the most important functions of EVs is the transfer of aforementioned bioactive molecules, which in cancer cells may affect tumor growth, progression, angiogenesis, and metastatic spread. Furthermore, EVs affect the presentation of antigens to immune cells via the transfer of nucleic acids, peptides, and proteins to recipient cells. Recent studies have also explored the potential application of EVs in cancer treatment. This review summarizes the mechanisms by which EVs regulate melanoma development, progression, and their potentials to be applied in therapy. We initially describe vesicle components; discuss their effects on proliferation, anti-melanoma immunity, and drug resistance; and finally focus on the effects of EV-derived microRNAs on melanoma pathobiology. This work aims to facilitate our understanding of the influence of EVs on melanoma biology and initiate ideas for the development of novel therapeutic strategies.
Highlights
Melanoma cells are exposed to bone-derived soluble factors, which are related to the molecular activation pathway of stromal-cell-derived factor 1 (SDF-1)/CXC chemokine receptor type 4 (CXCR4)/type 7 CXC chemokine receptor (CXCR7)
These results suggest that melanoma-cell-derived extracellular vesicles (EVs) contribute to melanoma metastasis
EVs regulate diverse cellular processes, and they contribute to cancer development and metastasis
Summary
Biological information between adjacent tumor cells can be transmitted through tumorderived EVs in a paracrine manner This signal transduction between malignant cells promotes cancer growth and metastasis and can interfere with normal signaling pathways [24]. Wnt Family Member 5A (WNT5A) regulates the release of EVs containing the immunomodulatory cytokine IL-6 and proangiogenic factors IL-8, VEGF, and MMP2 from melanoma cells (MeWo, SKmel, A2058, A375, and HTB63) This effect increases angiogenic processes and facilitates metastatic spread [31]. EVs derived from melanoma cells have been shown to increase type I interferon receptor (IFNAR1) and cholesterol 25-hydroxylase (CH25H) in normal cells, facilitating EV uptake and pre-metastatic niche development [35]. Plebanek et al suggested that cancerous cells are cleared at the pre-metastatic niche [41]
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