Fig. 9: Proposed model of resistance to immune response through FUT8-mediated aberrant N-glycosylation of B7H3 in TNBC cells. | Nature Communications

Fig. 9: Proposed model of resistance to immune response through FUT8-mediated aberrant N-glycosylation of B7H3 in TNBC cells.

From: FUT8-mediated aberrant N-glycosylation of B7H3 suppresses the immune response in triple-negative breast cancer

Fig. 9

In TNBC cells, FUT8 catalyzes aberrant B7H3 core fucosylation at N-linked oligosaccharides, which is essential for B7H3 stability and expression on the cell surface, resulting in the resistance of tumor cells to immune attack. Inhibition of B7H3 core fucosylation by 2F-Fuc reduces cell-surface expression of B7H3 and enhances T-cell activation, leading to more efficient tumor eradication.

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