MiRNAs are the most abundant non-coding RNAs enriched in EVs, and studies have also showed that EVs contain components of the RNA-induced silencing complex (RISC), suggesting potent regulatory role of EV-miRNA in recipient cells . Several studies have reported the regulation of signaling pathways in ECs by miRNAs delivered via tumor-derived EVs (Table 3). MiR-494 containing EVs secreted by tumor cells were taken up by ECs and promoted the migration of EC via targeting of PTEN and subsequent activation of Akt/eNOS pathway . EV-encapsulated miR-9 transferred from tumor cells to ECs reduced SOCS5 level, leading to JAK-STAT pathway activation to promote endothelial cell migration and sprout . Colorectal cancer cells secreted miR-1246 via EVs, which activated Smad1/5/8 signaling through targeting promyelocytic leukemia (PML) mRNA in recipient ECs, promoting angiogenic activities .Table 3MiRNAs involved in angiogenesis regulation by tumor-derived extracellular vesiclesmiRNAs in EVsTargetsFunctionRefmiR-494PTENpromote ECs migration, tube formationmiR-9SOCS5promote ECs migration, tube formationmiR-1246PMLpromote ECs proliferation, migration, tube formationmiR-23aPHD1, PHD2, ZO-1increase the number of tumor vessels, disrupt endothelial barriersmiR-210Ephrin-A3Promote ECs tube formationmiR-105ZO-1destroy tight junctions and integrity of vascular endothelial barriersSOCS5 suppressor of cytokine signaling 5, PML promyelocytic leukemia, PHD prolyl hydroxylase, ZO-1 tight junction protein 1