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Updated: Jul 2, 2026
11:36
Glycan Node Analysis: A Bottom-up Approach to Glycomics
Published on: May 22, 2016
N-Glycans in cancer progression
1Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, ON, Canada.
Glycobiology
|August 15, 2008
Summary
Altering N-glycan branching and metabolism can control cell surface receptor levels. This approach targets cancer by inducing growth arrest, offering a new therapeutic strategy.
Area of Science:
- Cell Biology
- Glycobiology
- Cancer Research
Background:
- N-glycan branching in the Golgi generates ligands for galectins, regulating cell surface glycoprotein levels like EGF and TGF-beta receptors.
- Glycoprotein N-glycan multiplicity interacts with metabolic flux and branching to control surface receptor expression.
Purpose of the Study:
- To investigate how N-glycan branching and metabolic flux influence cell surface receptor levels.
- To explore the role of beta1,6-N-acetylglucosaminyltransferase V (Mgat5) in oncogenesis and cancer progression.
- To propose a systems approach for cancer treatment targeting receptor surface distribution.
Main Methods:
- Analysis of N-glycan branching and multiplicity in glycoproteins.
- Investigating the role of Mgat5 in tumor cell metastasis and cytokine responsiveness.
- Examining changes in Caveolin-1 and reactive oxygen species in Mgat5-deficient tumor cells.
Main Results:
- Increased Mgat5 expression in oncogenesis promotes surface retention of growth receptors.
- Mgat5-deficient tumor cells exhibit reduced metastasis and cytokine responsiveness but altered proliferation pathways.
- Loss of Caveolin-1 and increased reactive oxygen species support tumor cell proliferation in Mgat5(-/-) cells.
Conclusions:
- Targeting cell surface receptor distribution via metabolism and N-glycan branching offers a potential cancer treatment strategy.
- Modulating N-glycan branching and UDP-GlcNAc levels can induce cancer cell growth arrest.
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