ArticleJournal of experimental & clinical cancer research : CR2026
Circulating extracellular vesicles from early-stage lung cancer patients trigger endothelial activation to drive pre-metastatic niche formation through synergistic miR-29a and C4A signaling.
Article in Journal of experimental & clinical cancer research : CR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMetastatic recurrence represents the major clinical challenge in early-stage lung cancer after curative surgery. Here, we investigated the role of circulating extracellular vesicles and particles (EVPs) in promoting formation of pre-metastatic niches (PMNs).
methodsPlasma-derived EVPs were obtained by ultracentrifugation from pre-surgery blood samples of patients with poor prognosis. Heavy-smokers cancer free individuals were used as control. EVP were characterized following MISEV guidelines. Functional experiments were carried out in vitro in 2D and 3D-bioprinted models as well as in vivo.
resultsEVPs from patients with early relapse show distinct molecular profiles, characterized by elevated levels of miR-29a and complement protein C4a. These EVPs preferentially target endothelial cells inducing a pro-inflammatory condition with upregulation of VCAM1 and CXCL1. In turn, endothelial modulation stimulated fibroblast activation and promoted neutrophils recruitment supporting PMNs formation. Mechanistically, we demonstrate that miR-29a and C4A act synergistically through SPARC down-modulation promoting cancer cell colonization. Preconditioning of mouse lungs using EVPs from patients with poor prognosis increased metastatic growth of human tumor cells, which was inhibited by miR-29a blockade.
conclusionsCirculating EVPs could be novel prognostic biomarkers and key players in PMN formation offering new targets to reduce relapses in lung cancer.
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