The FGF21 inhibitor inhibited HUVEC growth, migration, and invasion and significantly decreased eNOS, PI3K, and AKT mRNA levels and p-eNOS, PI3K, and p-AKT protein levels in HUVECs.
Furthermore, exogenous overexpression of miR‑335 and ‑543 significantly downregulated the expression level of eNOS, and substantially compromised the ability of migration and invasion in vitro.
Furthermore, a transwell insert invasion assay demonstrated that miR-155 inhibited cell invasion in trophoblast cells, and the effect was rescued by over expression of eNOS.
In either uninfected GBM cells or neural progenitor cells, thought to be the GBM precursor cells, HCMV infection or US28 overexpression was sufficient to promote secretion of biologically active VEGF and to activate multiple cellular kinases that promote glioma growth and invasion, including phosphorylated STAT3 (p-STAT3) and endothelial nitric oxide synthase (e-NOS).