TY - JOUR
T1 - Extracellular vesicle-derived miR21 of non-tumoral origin as early diagnostic marker of glioma
AU - De Luca, Mariassunta
AU - Rinaldi, Arianna
AU - Ioni, Arianna
AU - Oudin, Anaïs
AU - Scafidi, Andrea
AU - Poli, Aurélie
AU - Vilardo, Laura
AU - Golebiewska, Anna
AU - D’Agnano, Igea
AU - Michelucci, Alessandro
AU - Limatola, Cristina
AU - Catalano, Myriam
N1 - Funding:
This work was supported by Italian Ministry of Health (PNC SALUTE –
D3 4 Health − Digital Driven Diagnostics, prognostics and therapeutics
for sustainable Health care − PNC0001, Spoke 3 Linea tematica 2, CUP
B53C22006120001 to C.L.); Italian Ministry of University and Research
(PRIN-PNRR-P2022 × 5ESC to C.L.); by Associazione Italiana per la Ricerca sul
Cancro (AIRC2019-IG23010) to C.L.; Italian Ministry of Health (PON “RICERCA E
INNOVAZIONE” 2014–2020 - AZIONE IV.4 “DOTTORATI E CONTRATTI DI RICERCA
SU TEMATICHE DELL’INNOVAZIONE”) to M.C; Sapienza University of Rome
(RG123188B4236B9C) to M.C.
© 2025. The Author(s).
PY - 2025/12/2
Y1 - 2025/12/2
N2 - Background: Extracellular vesicles (EVs) are key elements in intercellular communication and are released into body fluids by all cells in physiological and pathological conditions. In brain tumors, EVs facilitate the bidirectional communication between neoplastic cells and the tumor microenvironment, promoting tumor progression and immune evasion. Among the various components of the EVs, microRNAs (miRs) act as potent regulators of gene expression. In particular, miR21 has gained attention as both a promising diagnostic biomarker and a key contributor to GBM progression. Methods: This study employed content analysis of miRs in EVs isolated from the brain, plasma, and urine of glioma-bearing mice. Results: Seven days after glioma cell injection, miR21 was the most highly expressed miR in both the brain and biofluids. Notably, its overexpression was particularly prominent in medium/large EVs. Co-culture experiments revealed that the early source of this marker is primarily microglia, rather than tumor cells. Conclusion: These data point out the potential of miR21 as early biomarker for glioma diagnosis and disease monitoring, emphasizing the role of non-tumoral cells, particularly microglia, as rapidly reacting elements in the context of gliomas.
AB - Background: Extracellular vesicles (EVs) are key elements in intercellular communication and are released into body fluids by all cells in physiological and pathological conditions. In brain tumors, EVs facilitate the bidirectional communication between neoplastic cells and the tumor microenvironment, promoting tumor progression and immune evasion. Among the various components of the EVs, microRNAs (miRs) act as potent regulators of gene expression. In particular, miR21 has gained attention as both a promising diagnostic biomarker and a key contributor to GBM progression. Methods: This study employed content analysis of miRs in EVs isolated from the brain, plasma, and urine of glioma-bearing mice. Results: Seven days after glioma cell injection, miR21 was the most highly expressed miR in both the brain and biofluids. Notably, its overexpression was particularly prominent in medium/large EVs. Co-culture experiments revealed that the early source of this marker is primarily microglia, rather than tumor cells. Conclusion: These data point out the potential of miR21 as early biomarker for glioma diagnosis and disease monitoring, emphasizing the role of non-tumoral cells, particularly microglia, as rapidly reacting elements in the context of gliomas.
KW - Extracellular vesicles
KW - Glioma
KW - Liquid biopsy
KW - MiR21
KW - Microglia
KW - Microglia/metabolism
KW - Humans
KW - Coculture Techniques
KW - Male
KW - Glioma/diagnosis
KW - Extracellular Vesicles/metabolism
KW - Animals
KW - Cell Line, Tumor
KW - Mice
KW - Brain Neoplasms/diagnosis
KW - MicroRNAs/metabolism
KW - Biomarkers, Tumor/metabolism
UR - https://www.scopus.com/pages/publications/105023570619
UR - https://pubmed.ncbi.nlm.nih.gov/41331452/
U2 - 10.1186/s12974-025-03605-1
DO - 10.1186/s12974-025-03605-1
M3 - Article
C2 - 41331452
AN - SCOPUS:105023570619
SN - 1742-2094
VL - 22
JO - Journal of Neuroinflammation
JF - Journal of Neuroinflammation
IS - 1
M1 - 282
ER -