Transfer of functional microRNAs between glioblastoma and microvascular endothelial cells through gap junctions.

Fiche publication

Date publication

novembre 2016




Membres identifiés du Cancéropôle Est :
Dr GARRIDO Carmen, Dr JEGO Gaëtan, Dr THURINGER Dominique, Mr PERNET Nicolas

Tous les auteurs :
Thuringer D, Boucher J, Jego G, Pernet N, Cronier L, Hammann A, Solary E, Garrido C


Extensive invasion and angiogenesis are hallmark features of malignant glioblastomas. Here, we co-cultured U87 human glioblastoma cells and human microvascular endothelial cells (HMEC) to demonstrate the exchange of microRNAs that initially involve the formation of gap junction communications between the two cell types. The functional inhibition of gap junctions by carbenoxolone blocks the transfer of the anti-tumor miR-145-5p from HMEC to U87, and the transfer of the pro-invasive miR-5096 from U87 to HMEC. These two microRNAs exert opposite effects on angiogenesis in vitro. MiR-5096 was observed to promote HMEC tubulogenesis, initially by increasing Cx43 expression and the formation of heterocellular gap junctions, and secondarily through a gap-junction independent pathway. Our results highlight the importance of microRNA exchanges between tumor and endothelial cells that in part involves the formation of functional gap junctions between the two cell types.

Mots clés

Cell Communication, genetics, Cell Line, Tumor, Endothelial Cells, metabolism, Gap Junctions, metabolism, Gene Expression, Glioblastoma, genetics, Humans, MicroRNAs, genetics, Neovascularization, Pathologic, genetics, RNA Transport


Oncotarget. 2016 Nov 8;7(45):73925-73934