fig1

Figure 1. Tumor-derived EVs exert various effects on ECs. Tumor-derived EV cargo molecules such as EGFR, VEGF-A, MMP13, VASN, miR-9, miR-205, and miR-210 are transported to ECs to induce the proangiogenic phenotype. miR-105, miR-181c, and miR-939 attenuate endothelial adhesion. miR-23a and miR-25-3p induce angiogenesis and disrupt the EC barrier, while TrpC5 and P-gp confer drug resistance to ECs. In addition, miR-1246 promotes tumor cell adhesion to ECs, disrupts the EC barrier, and confers drug resistance. EVs: Extracellular vesicles; ECs: endothelial cells; EGFR: epidermal growth factor receptor; VEGF-A: vascular endothelial growth factor A; MMP13: matrix metalloproteinase 13; VASN: vasorin.