Extracellular vesicles as mediators of exercise effects in cancer.
5 affiliations
- 1Department of Chemistry, LAQV-REQUIMTE, University of Aveiro, Aveiro, 3810-193, Portugal.
- 2Department of Medical Sciences, Institute of Biomedicine iBiMED, University of Aveiro, Aveiro, 3810-193, Portugal.
- 3Research Centre in Physical Activity, Health and Leisure (CIAFEL) and Laboratory for Integrative and Translational Research in Population Health (ITR), Faculty of Sports, University of Porto (FADEUP), Porto, 4200-450, Portugal.
- 4Department of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, Via Sommarive 9, Trento, 38123, Italy.
- 5Department of Medical Sciences, Institute of Biomedicine iBiMED, University of Aveiro, Aveiro, 3810-193, Portugal. [email protected].
Abstract
Exercise is a well-established non-pharmacological intervention in oncology, consistently associated with reduced cancer risk and improved disease outcomes. Yet, the molecular mechanisms through which physical activity exerts its anticancer effects remain incompletely understood. Extracellular vesicles (EVs) released in response to exercise have emerged as promising candidate mediators of these effects, acting as intercellular communication carriers that transport bioactive molecules modulating the tumor microenvironment and capable of interacting with distant tissues. The composition of EV cargo is highly sensitive to exercise modality, intensity, and physiological status. Aerobic and resistance exercise each elicit different EV molecular signatures that converge on key processes, including angiogenesis, immune surveillance, metabolic reprogramming, and inflammatory signaling. Preclinical data indicates that EVs obtained from exercised animals reduce tumor cell viability, impair proliferation and migration, induce apoptosis, and slow tumor progression in sedentary animals, positioning EVs as key mediators of exercise-induced tumor suppression. However, the contribution of different cellular origins, exercise protocol specificity, as well as biological sex to EV composition and anticancer function remain largely unresolved, limiting mechanistic interpretation and clinical translation. This review synthetizes the current evidence on the role of EVs released in response to exercise in cancer development and progression, identifies the key biological and methodological gaps impeding progress, and evaluates the translational challenges that must be overcome to harness their therapeutic potential in oncology.
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BibTeX
@article{aires2026extracellular,
title = {{Extracellular vesicles as mediators of exercise effects in cancer.}},
author = {Inês Aires and Daniel Moreira-Gonçalves and Vito G D'Agostino and Rita Ferreira and Rui Vitorino},
journal = {Molecular medicine (Cambridge, Mass.)},
year = {2026},
month = aug,
doi = {10.1186/s10020-026-01577-3},
url = {https://europepmc.org/article/MED/42958007},
note = {CC BY},
}
RIS
TY - JOUR
TI - Extracellular vesicles as mediators of exercise effects in cancer.
AU - Inês Aires
AU - Daniel Moreira-Gonçalves
AU - Vito G D'Agostino
AU - Rita Ferreira
AU - Rui Vitorino
PY - 2026
DA - 2026/08/01
JO - Molecular medicine (Cambridge, Mass.)
DO - 10.1186/s10020-026-01577-3
UR - https://europepmc.org/article/MED/42958007
AB - Exercise is a well-established non-pharmacological intervention in oncology, consistently associated with reduced cancer risk and improved disease outcomes. Yet, the molecular mechanisms through which physical activity exerts its anticancer effects remain incompletely understood. Extracellular vesicles (EVs) released in response to exercise have emerged as promising candidate mediators of these effects, acting as intercellular communication carriers that transport bioactive molecules modulating the tumor microenvironment and capable of interacting with distant tissues. The composition of EV cargo is highly sensitive to exercise modality, intensity, and physiological status. Aerobic and resistance exercise each elicit different EV molecular signatures that converge on key processes, including angiogenesis, immune surveillance, metabolic reprogramming, and inflammatory signaling. Preclinical data indicates that EVs obtained from exercised animals reduce tumor cell viability, impair proliferation and migration, induce apoptosis, and slow tumor progression in sedentary animals, positioning EVs as key mediators of exercise-induced tumor suppression. However, the contribution of different cellular origins, exercise protocol specificity, as well as biological sex to EV composition and anticancer function remain largely unresolved, limiting mechanistic interpretation and clinical translation. This review synthetizes the current evidence on the role of EVs released in response to exercise in cancer development and progression, identifies the key biological and methodological gaps impeding progress, and evaluates the translational challenges that must be overcome to harness their therapeutic potential in oncology.
SN - 1076-1551
SN - 1528-3658
ER -