ArticlePloS one2026
Neuroblastoma cell growth and invasiveness is modulated by the activity of N-acetylglucosaminyltransferase-III.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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3 authors.
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Abstract
The presence of complex N-glycans with β1,6-N-acetylglucosamine (GlcNAc) on cells has long been associated with cancer. For this reason, the role of N-acetylglucosaminyltransferase-III (GnT-III, MGAT3) to hinder terminal N-glycan processing by the addition of β1,4-GlcNAc residues (bisected N-glycan), has earned GnT-III a reputation as a tumor suppressor. In this study, by the creation and characterization of human MGAT3 knockout in the Be(2)-C cell line, a NB cell line, (MGAT3-/-), we solidify GnT-III activity as a suppressor of NB progression by showing that the loss of GnT-III coincided with increased cell proliferation and cell spheroid invasion, along with cell migration, and cell-cell adhesion, and modified cell types. Lectin blotting results indicated that bisected N-glycans were greatly diminished in MGAT3-/-. Further GNL and L-PHA binding suggested that oligomannose and β1,6-GlcNAc branched N-glycans were raised in MGAT3-/- relative to the BE(2)-C cell line. Cellular phenotypes of MGAT3-/- could be rescued by transient expression of Mgat3 cDNA. Likewise, altered levels of bisecting GlcNAc N-glycans in a rat NB cell line (NB_1) overexpressing GnT-III had reduced cell-cell adhesion, cell migration, and cell invasiveness. We conclude that lowered GnT-III activity promotes cell invasiveness and growth in NB, and speculate that oligomannose and β1,6-GlcNAc branched N-glycans are key determinants.
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