pipette
ENEnglish

Neuroblastoma-derived small extracellular vesicles retaincellular identity and adrenergic/mesenchymal state signatures

M. Grimaldi, M. Kirchner, A. Szymansky, A. Hendrix, A. Muenster-Wandowski, H. Gerhardt, A. H. Hagemann, M. Lodrini, M. Auber, P. Mertins, H. E. Deubzer

PreprintAfirmaciones fuertes, leer con cuidado

En palabras de los autores

Neuroblastoma is a heterogeneous pediatric malignancy characterized by distinct genomic subgroups and cell-state plasticity between adrenergic (ADRN) and mesenchymal (MES) phenotypes. While small extracellular vesicles (sEVs) mediate pre-metastatic niche priming, the degree to which sEV proteomes reflect parental genomic and phenotypic identity remains unresolved. Here, we isolated sEVs from six neuroblastoma cell models (IMR-5/75, BE(2)-C, GI-ME-N, CLB-GA, LAN-6, and SK-N-FI) representing three genomic subgroups (MYCN-amplified, TERT-rearranged, and unaltered) using OptiPrep density gradient centrifugation followed by size exclusion chromatography and ultrafiltration. High-resolution mass spectrometry of sEV proteomes revealed that sEVs carry highly reproducible protein signatures that tightly correlate with the parental genomic subgroups. Analyzing paired cell/sEV samples, we demonstrate cell-to-EV concordance of lineage-specific markers: ADRN sEVs selectively enriched L1CAM and dopamine {beta}-hydroxylase (DBH), whereas MES sEVs enriched SERPINE1 and type III collagen (COL3A1). These findings indicate that neuroblastoma-derived sEVs systematically preserve both the genomic landscape and the lineage transdifferentiation states of their cells of origin. This study establishes a robust molecular foundation for utilizing sEV-based proteomics as a surrogate to track cellular plasticity and for studying sEV-mediated microenvironmental remodeling.

Resultado principalEl resumen no menciona limitaciones.

Apareció: miércoles, 23 de septiembre. bioRxiv. Preprint, todavía sin revisión por pares.

DOI: 10.64898/2026.09.21.753086