Within this pathway, our glycoproteomic data provided substantial evidence to reveal that the folate uptake capacity of FOLR1 can be positively regulated by site-specific core-fucosylation attached at FOLR1, which established a direct connection between the overexpression of FUT8 (and increased core-fucosylation) induced by HGF or TGF-β1 and the EMT of cancer cells stimulated by “super-physiological” dose of folate, which were only reported disjointly in previous studies 36-38. Here, HGF is linked to cancer.