Anticancer Therapy-Induced Alterations in Tumor-Derived Extracellular Vesicles: Molecular Mechanisms and Biological Effects
- 1Department of Biological Science, Immunology Research Lab & BK21-Four Educational Research Group for Age-Associated Disorder Control Technology, Chosun University, Gwangju 61452, Republic of Korea
Abstract
Anticancer treatment alters the secretion and molecular composition of tumor-derived extracellular vesicles (EVs). Chemotherapy, ionizing radiation, and molecularly targeted therapy are associated with changes in EV-associated microRNAs (miRNAs), circular RNAs (circRNAs), long non-coding RNAs (lncRNAs), small nuclear RNAs (snRNAs), proteins, metabolic components, and tumor-associated antigens. Some treatment-associated EV changes are supported by molecular characterization alone, whereas others have been evaluated for functional effects in recipient cells. At the donor-cell level, altered EV release and cargo loading involve RAB family small GTPases, lysosomal degradation, multivesicular body–plasma membrane fusion mediated by soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins, the exocyst component Exo70, and RNA- and protein-loading processes. In recipient tumor cells, reported responses include changes in WNT/β-catenin and NOTCH signaling, phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), mitogen-activated protein kinase (MAPK), platelet-derived growth factor receptor α (PDGFRα) signaling, glutamine metabolism, and oxidative responses. Evidence supporting individual cargo–response relationships includes both association-based observations and perturbation-based functional validation. In immune cells, C-X-C motif chemokine ligand 1 (CXCL1)-containing EVs increase programmed death-ligand 1 (PD-L1) expression in macrophages, and PD-L1-positive small extracellular vesicles (sEVs) reduce CD8+ T-cell proliferation and granzyme B production, whereas radiation-induced sEVs carrying tumor-associated antigens and heat shock proteins increase antigen presentation and CD4+ and CD8+ T-cell responses. This review separates treatment-associated molecular EV alterations from experimentally evaluated recipient-cell effects to clarify the evidence supporting therapy-induced EV responses.
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BibTeX
@article{kim2026anticancer,
title = {{Anticancer Therapy-Induced Alterations in Tumor-Derived Extracellular Vesicles: Molecular Mechanisms and Biological Effects}},
author = {Mi Eun Kim and Jun Sik Lee},
journal = {Molecules},
year = {2026},
month = oct,
doi = {10.3390/molecules31213901},
url = {https://www.mdpi.com/1420-3049/31/21/3901},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Anticancer Therapy-Induced Alterations in Tumor-Derived Extracellular Vesicles: Molecular Mechanisms and Biological Effects
AU - Mi Eun Kim
AU - Jun Sik Lee
PY - 2026
DA - 2026/10/29
JO - Molecules
DO - 10.3390/molecules31213901
UR - https://www.mdpi.com/1420-3049/31/21/3901
AB - Anticancer treatment alters the secretion and molecular composition of tumor-derived extracellular vesicles (EVs). Chemotherapy, ionizing radiation, and molecularly targeted therapy are associated with changes in EV-associated microRNAs (miRNAs), circular RNAs (circRNAs), long non-coding RNAs (lncRNAs), small nuclear RNAs (snRNAs), proteins, metabolic components, and tumor-associated antigens. Some treatment-associated EV changes are supported by molecular characterization alone, whereas others have been evaluated for functional effects in recipient cells. At the donor-cell level, altered EV release and cargo loading involve RAB family small GTPases, lysosomal degradation, multivesicular body–plasma membrane fusion mediated by soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins, the exocyst component Exo70, and RNA- and protein-loading processes. In recipient tumor cells, reported responses include changes in WNT/β-catenin and NOTCH signaling, phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), mitogen-activated protein kinase (MAPK), platelet-derived growth factor receptor α (PDGFRα) signaling, glutamine metabolism, and oxidative responses. Evidence supporting individual cargo–response relationships includes both association-based observations and perturbation-based functional validation. In immune cells, C-X-C motif chemokine ligand 1 (CXCL1)-containing EVs increase programmed death-ligand 1 (PD-L1) expression in macrophages, and PD-L1-positive small extracellular vesicles (sEVs) reduce CD8+ T-cell proliferation and granzyme B production, whereas radiation-induced sEVs carrying tumor-associated antigens and heat shock proteins increase antigen presentation and CD4+ and CD8+ T-cell responses. This review separates treatment-associated molecular EV alterations from experimentally evaluated recipient-cell effects to clarify the evidence supporting therapy-induced EV responses.
SN - 1420-3049
ER -