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. 2023 Jan 6;12:1093496. doi: 10.3389/fonc.2022.1093496

Figure 1.

Figure 1

Formation of truncated O-glycans in tumors modulates cell-intrinsic behavior and interactions with the tumor immune microenvironment. (A). O-glycosylation in human cells involves highly regulated sequential reactions catalyzed by glycosyltransferases. (B). Mechanisms mediating loss of O-glycan chain extension (mentioned in red) facilitate neoplastic transformation, increase oncogenic signaling cascades, the epithelial-to-mesenchymal transition process, and compromise death receptor stability to evade apoptosis. The Tn/STn antigens interact with macrophage-galactose lectin (MGL) and CD206 (mannose receptor), expressing tumor-associated macrophages (TAMs); natural killer (NK) cells; and monocytic dendritic cells - preventing their maturation, leading to an overall immunosuppressed microenvironment. [ppGalNAc-T, polypeptide-GalNActransferase; C1GalT1, core1 β3-galactosyltransferase; COSMC, Core1-Specific-Molecular-Chaperone; C2GnT, core2 β1,6 N-acetylglucosaminyltransferase; β3GnT6, β-1,3-N-Acetylglucosaminyltransferase; ST6GalNAc-1, α2,6 sialyltransferase; ST3Gal-1, α2,3 sialyltransferase; PDAC, pancreatic ductal adenocarcinoma].