Fig. 7

Schematic representation of MT-mediated FGF19 signaling in HNSCC cells. High-dose MT has the potential to upregulate FGF19 gene expression through activating ER stress-responsive PERK-eIF2α-ATF4 signaling in HNSCC cells. Increased FGF19 is secreted and then recruited back to cells by its specific receptor FGFR4 and further activates Vimentin signaling, which in turn confines the role of MT in anti-metastasis