ArticleMolecular and cellular pediatrics2026
O-GlcNAcylation expression predicts a favorable prognosis and mitigates malignant phenotypes via MYCN suppression in neuroblastoma.
Article in Molecular and cellular pediatrics, 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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1 citing paper in PubMed.
- O-GlcNAcylation at the tumor-immune interface: a metabolic post-translational code driving immune evasion and therapy resistance in cancer.Frontiers in immunology · 2026Review
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10 authors.
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Abstract
backgroundNeuroblastoma (NB) is a common pediatric malignancy originating from neural crest progenitor cells. While O-GlcNAcylation is known to regulate cancer cell metabolism and behavior, its specific role and prognostic value in neuroblastoma remain poorly understood. This study aims to elucidate the clinical significance and molecular mechanisms of O-GlcNAcylation in NB.
methodsWe analyzed O-GlcNAcylated protein expression in 158 human NB tumor samples using immunohistochemistry (IHC) and correlated the findings with clinicopathological parameters and survival outcomes. The therapeutic potential of enhancing O-GlcNAcylation via the OGA inhibitor Thiamet G was evaluated in MYCN-amplified NB cell lines and the Th-MYCN transgenic mouse model. Molecular mechanisms governing MYCN stability were investigated using Western blotting, immunoprecipitation, and functional assays.
resultsHigh levels of O-GlcNAcylated proteins were significantly associated with differentiated histology and early clinical stages. Survival analysis identified high O-GlcNAc expression as an independent prognostic factor for favorable outcomes. In vitro and in vivo experiments demonstrated that Thiamet G treatment effectively suppressed tumor growth and invasion while promoting neuronal differentiation. Mechanistically, Thiamet G-induced O-GlcNAc accumulation reduced inhibitory phosphorylation of GSK3β at Ser9, thereby activating GSK3β. This activation promoted the phosphorylation of MYCN at Thr58, accelerating its degradation via the ubiquitin-proteasome pathway.
conclusionOur findings demonstrate that high O-GlcNAcylated protein levels predict a favorable prognosis in neuroblastoma. Pharmacological inhibition of OGA with Thiamet G destabilizes the MYCN oncoprotein via the GSK3β-proteasome axis, suppressing tumorigenesis and inducing differentiation. This suggests that modulating O-GlcNAc levels represents a promising therapeutic strategy for MYCN-driven neuroblastoma.
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