Exosomes, nano-sized extracellular vesicles secreted by all varieties of living cells, have emerged as pivotal mediators of intercellular communication within the tumor microenvironment. While exosomes significantly contribute to tumor progression, metastasis, immune modulation, and resistance to therapy, the mechanisms of cargo selection and clinical translation remain controversial and insufficiently resolved. Recent high-throughput technologies have enabled detailed profiling of exosomal cargo; however, substantial challenges persist in their clinical application due to issues in isolation and standardization. This review systematically dissects these molecular biogenesis controversies, the roles of tumor-derived exosomes in modulating angiogenesis, immune escape, metastasis, and therapy resistance, and critically evaluates barriers hindering their clinical adoption.

Messaging malignancy: Tumour-derived exosomes at the nexus of immune escape, vascular remodelling and metastatic competence

Beccari, Tommaso;Pascucci, Luisa;
2025

Abstract

Exosomes, nano-sized extracellular vesicles secreted by all varieties of living cells, have emerged as pivotal mediators of intercellular communication within the tumor microenvironment. While exosomes significantly contribute to tumor progression, metastasis, immune modulation, and resistance to therapy, the mechanisms of cargo selection and clinical translation remain controversial and insufficiently resolved. Recent high-throughput technologies have enabled detailed profiling of exosomal cargo; however, substantial challenges persist in their clinical application due to issues in isolation and standardization. This review systematically dissects these molecular biogenesis controversies, the roles of tumor-derived exosomes in modulating angiogenesis, immune escape, metastasis, and therapy resistance, and critically evaluates barriers hindering their clinical adoption.
2025
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11391/1616895
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