TNF-α treatment activated the kinase activity of FAK and its phosphorylation especially at Y397 and Y925. Conditional expression of wild-type FAK in FAK-null cells restored the TNF-α–dependent production of MMP-9. In contrast, FAK-null fibroblasts could not respond well to TNF-α stimulation. TNF-α stimulation of CCKS1 or wild-type fibroblasts substantially activated FAK phosphorylation and increased MMP-9 production. We investigated the role of focal adhesion kinase (FAK) in TNF-α–dependent production of MMP-9 in CCKS1 and FAK-null mouse fibroblast cells. dissemination, dramatically increased matrix metalloproteinase-9 (MMP-9) production and tumor invasion. We have previously reported that tumor necrosis factor-α (TNF-α) stimulation of CCKS1, a cell line established from cholangiocarcinoma with i.p.
0 kommentar(er)
