PT - JOURNAL ARTICLE AU - PO-JUNG PAN AU - JAI-JEN TSAI AU - YU-CHANG LIU TI - Amentoflavone Inhibits Metastatic Potential Through Suppression of ERK/NF-κB Activation in Osteosarcoma U2OS Cells DP - 2017 Sep 01 TA - Anticancer Research PG - 4911--4918 VI - 37 IP - 9 4099 - http://ar.iiarjournals.org/content/37/9/4911.short 4100 - http://ar.iiarjournals.org/content/37/9/4911.full SO - Anticancer Res2017 Sep 01; 37 AB - Aim: The study goal was to investigate effect of amentoflavone on nuclear factor-κB (NF-κB)-modulated metastatic mechanism in osteosarcoma U2OS cells. U2OS cells were treated with amentoflavone, NF-κB inhibitor, protein kinase B (PKB or AKT) inhibitor or mitogen-activated protein kinase (MAPK) inhibitor. Change of cell viability, NF-κB 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-κB 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-κB-modulated metastatic mechanism. Amentoflavone significantly inhibited NF-κB 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-κB activation in osteosarcoma U2OS cells.