Transfected U87 were double loaded with calcein, a dye that passes through gap junctions, and DiL, a membrane-bound dye (Figure 3A; ). Labelled U87 were plated onto HMEC monolayers to which they rapidly adhered. The calcein transfer to HMEC was then measured, attesting the formation of heterocellular GJIC. When U87 were transfected with a miR-5096 mimic, calcein transfer was significantly increased within 5 hours. The gap junction blocker, carbenoxolone, did not affect cancer cell adhesion to endothelial cells (Figure 3A), but abolished calcein transfer from U87 to HMEC (Figure 3B). A similar result was obtained by inhibiting miR-5096 expression in glioblastoma cells. These results suggest that miR-5096 itself favors the communication between cancer and endothelial cells.