Effect of extracellular vesicles on malignant tumours: Mechanisms and clinical findings (Review)

Extracellular vesicles (EVs) are critical mediators of intercellular communication within the tumour microenvironment (TME). EVs carry bioactive cargo, including proteins, nucleic acids and lipids, that modulate tumourigenesis, progression and therapeutic resistance via a range of molecular and cellular mechanisms. As natural carriers of functional biomolecules, EVs contribute to key oncogenic processes, including tumour cell proliferation, invasion, immune evasion and drug resistance. Notably, EVs secreted by cancer cells harbour tumour‑specific molecular signatures, such as oncoproteins, non‑coding RNAs and mutant transcripts, thereby facilitating microenvironmental reprogramming and malignant evolution. The present review systematically examines five key molecular mechanisms by which tumour‑derived EVs promote malignant progression: i) Remodelling of the extracellular matrix and organ‑specific metastasis through the delivery of metastasis‑associated proteins such as matrix metalloproteinases and integrins; ii) induction of immune cell exhaustion and tumour immune evasion through the release of immunosuppressive molecules, including programmed death ligand 1 and transforming growth factor‑β; iii) establishment of tumour neovascular networks through the delivery of pro‑angiogenic factors such as vascular endothelial growth factor; iv) reprogramming of the metabolic landscape of the TME through the encapsulation of key enzymes involved in glycolysis and lipid metabolism; and v) mediation of resistance to chemotherapy and targeted therapy through the transport of ATP‑binding cassette transporters, inhibitor of apoptosis proteins and other molecules. On this basis, the present review focuses on the unique advantages of EVs as novel liquid biopsy biomarkers for early tumour diagnosis, therapeutic efficacy monitoring and prognostic evaluation, as well as the application prospects of engineered EVs as targeted drug delivery systems for precision tumour therapy. The core conclusion is that the major bottlenecks currently restricting the clinical translation of EVs include the lack of standardised isolation and identification methods, the unclear regulatory mechanisms underlying EV heterogeneity and the low efficiency of targeted in vivo delivery. Future research should focus on dissecting the functional specificity of EV subpopulations and performing precision‑engineering modifications of EVs, thereby providing new strategic directions for overcoming tumour therapeutic resistance and immune evasion.