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Transfer of functional microRNAs between glioblastoma and microvascular
endothelial cells through gap junctions
#MMPMID27661112
Thuringer D
; Boucher J
; Jego G
; Pernet N
; Cronier L
; Hammann A
; Solary E
; Garrido C
Oncotarget
2016[Nov]; 7
(45
): 73925-73934
PMID27661112
show ga
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.
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