Tyrosine kinase receptors VEGFR and platelet-derived growth factor receptor (PDGFR) are primarily located on the surface of ECs [80, 81]. The binding of VEGF-A to VEGFR-2 and PDGF to PDGFR initiates a cascade of signals that result in endothelial cell proliferation and migration . Several miRNAs have been reported to directly target these receptors in ECs, such as miR-128  and miR-497 , blocking their downstream signaling to inhibit tumor angiogenesis. On the contrary, miRNAs targeting the suppressors of these receptors promoted tumor angiogenesis. MiR-296 contributed to angiogenesis by directly targeting the hepatocyte growth factor-regulated tyrosine kinase substrate (HGS) mRNA, thereby reducing HGS-mediated degradation of VEGFR-2 and PDGFRβ in ECs . MiR-146a enhanced tumor angiogenesis by targeting BRCA1 which conferred a transcriptional repression on PDGFRA .