Fig. 6

EVs-miR-182-5p induces proliferation, migration and angiogenesis of HUVECs through inhibition of CMTM7 and activation of the EGFR/AKT signaling pathway. A Venn diagram of genes related to CMTM7 expression in breast cancer tissue samples from dataset GSE50428, MEM database and LinkedOmics database; B PPI network of 98 intersection genes related to CMTM7 expression constructed using String (in the PPI network, the higher core degree is, the more red the circle color is; otherwise, the lower the core degree, the bluer the color is); C Expression of CMTM7, VEGF, p-EGFR, EGFR, p-AKT and AKT in HUVECs treated with EVs or combined with miR-182-5p inhibitor by Western blot analysis, the statistical power was 1; D Expression of CMTM7, VEGF, p-EGFR, EGFR, p-AKT and AKT in HUVECs treated with EVs or combined with GDC0068 detected by Western blot analysis, the statistical power was 1; E Proliferation of HUVECs treated with EVs or combined with GDC0068 detected by CCK-8 method, the statistical power was 1; F Migration of HUVECs treated with EVs or combined with GDC0068 detected by scratch test, the statistical power was 1; G Migration ability of HUVECs treated with EVs or combined with GDC0068 detected by Transwell assay, the statistical power was 1; H Vessel-like tube formation in vitro of HUVECs treated with EVs or combined with GDC0068, the statistical power was 1. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 compared with control HUVECs, or HUVECs treated with PBS or EVs + inhibitor NC. #p < 0.05, ##p < 0.01, ###p < 0.001 compared with HUVECs treated with DMSO-EVs. The experiment was conducted three times independently