Fig. 3
From: Protein glycosylation in cancers and its potential therapeutic applications in neuroblastoma
Altered glycans and related pathophysiological events involved in NB progression. a β1,4-N-acetylgalactosaminyltransferase 3 (B4GALNT3) and β1,4-galactosyltransferase 3 (B4GALT3) exhibit differential effects on malignant phenotypes by modification of β1 integrin in NB cells; b N-acetylgalactosaminyltransferase 2 (GALNT2) modifies O-glycans on IGF-1R, thereby suppressing IGF-1-induced IGF-1R dimerization and downstream signaling; c N-acetylglucosaminyltransferase V (GnT-V) modulates the sensitivity of NB to apoptosis; d Gal-1 promotes attachment of NB cells to the extracellular matrix (ECM) and endothelial cells through binding to CD44. Besides, Gal-1 may dampen the function of T cells and dendritic cells as well. Glycosaminoglycans present as e free polysaccharides (hyaluronic acid), a major counterreceptor for f CD44, or g as part of proteoglycans (heparan sulfate and chondroitin sulfate). GalNAc N-acetylgalactosamine, GlcNAc N-acetylglucosamine, Gal galactose, NeuAc, N-acetylneuraminic acid, Fuc fucose, Glc glucose, Man mannose, Xyl xylose, GlcA glucuronic acid, IdoA iduronic acid