Amentoflavone Inhibits Metastatic Potential.hrough Suppression of ERK/NF-κB Activation in Osteosarcoma U2OS Cells

Aim: The study goal was to investigate effect of amentoflavone on nuclear factor-kappa B (NF-kappa B)-modulated metastatic mechanism in osteosarcoma U2OS cells. U2OS cells were treated with amentoflavone, NF-kappa B inhibitor, protein kinase B (PKB or AKT) inhibitor or mitogen-activated protein kinase (MAPK) inhibitor. Change of cell viability, NF-kappa B activation, expression of metastasis-associated proteins, signal transduction, and cell migration and invasion were evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, NF-kappa B reporter gene assay, western blotting, and cell migration and invasion assays. The results demonstrated that inhibition of activation of extracellular signal-regulated kinases (ERK) was a key point for suppression of NF-kappa B-modulated metastatic mechanism. Amentoflavone significantly inhibited NF-kappa B activation, ERK phosphorylation, expression of metastasis-associated proteins, and cell migration and invasion. Our findings indicate that amentoflavone reduces metastatic potential through suppression of ERK and NF-kappa B activation in osteosarcoma U2OS cells.