Accumulated evidence indicate that non-coding microRNAs (miRs) have multiple effects on gene regulation during tumor progression [14, 21]. Here, we demonstrate the ability of gap junctions to drive miRs exchange between HMEC and the U87 human glioblastoma cell line and to modulate the behavior of target cells. First, miR-145, which is downregulated in early stages of glioma progression  and behaves as a tumor suppressor , can migrate from endothelial to tumor cells and function as an “antiangiogenic” signal. Second, miR-5096, which is upregulated in glioma (as compared to normal brain tissues) and promotes glioma invasion , can migrate from tumor cells to endothelial cells in which it functions as a “proangiogenic” signal. The cell-to-cell transfer of these miRs is inhibited by the loss of contact between HMEC and U87 cells and by the presence of the GJIC blocker, carbenoxolone, indicating that miR-145 and miR-5096 use the same intercellular transfer pathway (GJIC) to mediate their opposite effects on angiogenesis.