MiR-17-3p inhibits angiogenesis by downregulating flk-1 in the cell growth signal pathway

MicroRNAs (miRs) are endogenously expressed small noncoding RNAs that regulate gene expression at the posttranscriptional level. Previous works indicated that the miR-17-92 cluster could regulate endothelial cell (EC) functions involved in angiogenesis. miR-17-3p, a component of the miR-17-92 cluster, could control the angiogenic activity of human umbilical vein ECs in a cell-autonomous manner in vitro. A 21-bp fragment from the Flk-1 3'-untranslated region containing miR-17-3p targeting sites was required for the rapid downregulation of Flk-1 expression by in silico and experimental analysis. Subsequently, the downstream cell growth pathway was inhibited by forced upregulation of miR-17-3p. Based on these data, we conclude that miR-17-3p is a negative regulator of the angiogenic phenotype of ECs through its ability to modulate the expression of Flk-1, which is implicated in the pleiotropic effects of miR-17-92 in angiogenesis.