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. 2017 Nov 3;9(1):1380–1402. doi: 10.18632/oncotarget.22377

Figure 2. Specific alterations of glycosylation in colorectal cancer.

Figure 2

The HBP pathway produces the nucleotide sugar UDP-GlcNAc in a nutrient-dependent manner. UDP-GlcNAc is critical for most kinds of glycosylation including N-glycosylation, O-GalNAc-based glycosylation and O-GlcNAcylation. In this sense, glycan structures are modified according to the metabolic status of the cell. The abnormal glycosylation which occurs in cancer cells can be attributed to abundance and availability of nucleotide sugars, acceptor substrates or cofactors in the same way as altered expression or activity, or mislocalization of glycosyltransferases. The most frequent abnormal glycosylations observed in CRC are increased branched- and sialylated-N-glycans, truncated mucin-type O-glycans, increased fucosylation and sialylation of Lewis antigens and increased O-GlcNAcylation. Green and red arrows indicate respectively increased and decreased availability of nutrients and nucleotide sugars, or expression or activity of glycosyltransferases in CRC. Acetyl-coA: acetyl-coenzyme A; Fru-6-P: fructose-6-phosphate; Glc-6-P: glucose-6-phosphate; GlcN-6-P: glucosamine-6-phosphate; GlcNAc-6-P: N-acetylglucosamine-6-phosphate; GlcNAc-1-P: N-acetylglucosamine-1-phosphate; Glu: glutamic acid; UTP: uridine triphosphate; PPi: inorganic pyrophosphate.