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Glycosynaptic microdomains controlling tumor cell phenotype through alteration of cell growth, adhesion, and motility Hakomori SIFEBS Lett 2010[May]; 584 (9): 1901-6Glycosphingolipids (GSLs) GM3 (NeuAcalpha3Galbeta4Glcbeta1Cer) and GM2 (GalNAcbeta4[NeuAcalpha3]Galbeta4Glcbeta1Cer) inhibit (i) cell growth through inhibition of tyrosine kinase associated with growth factor receptor (GFR), (ii) cell adhesion/motility through inhibition of integrin-dependent signaling via Src kinases, or (iii) both cell growth and motility by blocking "cross-talk" between integrins and GFRs. These inhibitory effects are enhanced when GM3 or GM2 are in complex with specific tetraspanins (TSPs) (CD9, CD81, CD82). Processes (i)-(iii) occur through specific organization of GSLs with key molecules (TSPs, caveolins, GFRs, integrins) in the glycosynaptic microdomain. Some of these processes are shared with epithelial-mesenchymal transition induced by TGFbeta or under hypoxia, particularly that associated with cancer progression.|*Cell Proliferation[MESH]|Animals[MESH]|Cell Adhesion/physiology[MESH]|Cell Movement/*physiology[MESH]|Glycosphingolipids/metabolism/*physiology[MESH]|Humans[MESH]|Membrane Microdomains/metabolism/*physiology[MESH]|Membrane Proteins/metabolism/physiology[MESH]|Models, Biological[MESH]|Neoplasms/metabolism/*pathology[MESH]|Phenotype[MESH] |
