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Glycosynaptic microdomains controlling tumor cell phenotype through alteration of cell growth, adhesion, and motility
Author(s) -
Hakomori Sen-itiroh
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.10.065
Subject(s) - microbiology and biotechnology , motility , lipid microdomain , integrin , cell adhesion , biology , cell growth , receptor tyrosine kinase , cell adhesion molecule , focal adhesion , kinase , tyrosine kinase , cell , signal transduction , chemistry , biochemistry , membrane
Glycosphingolipids (GSLs) GM3 (NeuAcα3Galβ4Glcβ1Cer) and GM2 (GalNAcβ4[NeuAcα3]Galβ4Glcβ1Cer) 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 TGFβ or under hypoxia, particularly that associated with cancer progression.