We subsequently used an in vitro matrigel tube formation assay to explore if miR-5096 could modulate the ability of HMEC to form capillary-like structures . Co-culture of U87 and HMEC initiated the formation of typical capillary-like structures within 5 hours (Figure 4A). When miR-5096 mimic-loaded U87 were co-cultured with HMEC, the formation of a capillary-like network at 5 hours was increased (Figure 4A, 4B). Such an effect was not observed when U87 were loaded with a miR-5096 specific inhibitor. Thus, miR-5096 expressed by glioblastoma cells could act as a proangiogenic factor, i.e., through increasing tubulogenesis (Figure 4B). The opposite effect was observed when miR-145-5p mimic-transfected HMEC were co-cultured with U87, as this transfection inhibited the formation of capillary-like structures (Figure 4B, see supplementary Figure S1). Altogether, these results suggest that, by modulating the tumor associated capillary-like network, the transfer of miR-145-5p from endothelial to cancer cells may decrease tumor growth whereas the transfer of miR-5096 from cancer to endothelial cells may have opposite effects by promoting angiogenesis.