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Glycobiology Advance Access published online on August 13, 2008
Glycobiology, doi:10.1093/glycob/cwn071
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© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

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N-glycans in Cancer Progression

Ken Lau1,3 and James W. Dennis1,2

1 Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Avenue R988, Toronto, Ontario, M5G 1X5, Canada Phone: 416–586-8233 FAX: 416–586-8587 Email: mailto:dennis{at}mshri.on.ca
2 Departments of Molecular Genetics, Laboratory Medicine and Pathology, University of Toronto, ON
3 Departments of Biochemistry, University of Toronto, ON

Received on May 5, 2008; accepted on July 27, 2008

N-glycan branching in the medial Golgi generates ligands for lattice-forming lectins (eg. galectins) that regulate surface levels of glycoproteins including EGF and TGF-β receptors. Moreover, functional classes of glycoproteins differ in N-glycan multiplicities (number of N-glycans/peptide), a genetically-encoded feature of glycoproteins that interacts with metabolic flux (UDP-GlcNAc) and N-glycan branching to differentially regulate surface levels. Oncogenesis increases β1,6-N-acetylglucosaminyltransferase V (encoded by Mgat5) expression, and its high-affinity galectin ligands promote surface retention of growth receptors with a reduced dependence on UDP-GlcNAc. Mgat5–/- tumor cells are less metastatic in vivo and less responsive to cytokines in vitro, but undergo secondary changes that support tumor cell proliferation. These include loss of Caveolin-1, a negative regulator of EGF signaling, and increased reactive oxygen species, an inhibitor of phosphotyrosine phosphatases. These studies suggest a systems approach to cancer treatment where the surface distribution of receptor is targeted though metabolism and N-glycan branching to favor growth arrest.


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