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. 2021 Jan 26;4:119. doi: 10.1038/s42003-020-01642-5

Fig. 7. Circulating miR-424-loaded EVs are oncogenically active in mouse models and human patients.

Fig. 7

A Schematic plan for in vivo assessment of EVs functionality. B In vivo imaging of distribution of DiD-labeled EVs from control (EVs-CTRL) and miR-424 expressing (EVs-424) donor cells 24 h after intravenous injection to NSG mice with RWPE-1 xenografts. C Growth of RWPE-1 xenografts following single tail vein injection of EVs-CTRL and EVs-424 (n = 4/group). D miR-424 level in RWPE-1 xenografts in mice injected with EVs-CTRL and EVs-424. E Assessment of protein markers by IHC in RWPE-1 xenografts from mice injected with EVs-CTRL and EVs-424. Right, IHC scores for each protein markers. F Functional assessment of patient-derived EVs in recipient RWPE-1 cells. G Confocal microscopy images of RWPE-1 cells supplemented with patient-derived EVs stained with PKH26 (red). H Tumor-sphere forming assay of RWPE-1 cells supplemented with EVs derived from the indicated patient groups. Bottom, representative images of tumor-spheres. I Tumor-sphere forming efficiency of recipient cells as in H shown in relation to miR-424 status after supplementation of patient-derived EVs. *p ≤ 0.05, **p ≤ 0.01 by two-tailed Student’s t-test. Following on reports that miR-424 expression promotes oncogenesis, Domenico Albino et al. find that extracellular vesicles (EVs) in the plasma of prostate cancer patients secrete miR-424. Using cell-based and animal models, they demonstrate that EV-mediated release of miR-424 can transfer oncogenic signals across cells to promote recurrence and metastatic progression.