ArticleCell chemical biology2025
Redundancy of the OST catalytic subunit facilitates therapeutic targeting of N-glycosylation.
Article in Cell chemical biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- The Oligosaccharyltransferase Catalytic Subunit PsSTT3B Is Required for Asexual Development and Pathogenicity inJournal of fungi (Basel, Switzerland) · 2026Article
- STT3A-mediated FCN3 N-glycosylation promotes Treg cell activation to drive hepatocellular carcinoma progression via Wnt/β-catenin.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Oligosaccharyltransferase (OST) complex inhibition effectively treats rodent and human prions.PLoS pathogens · 2026Article
- Constructing a Prognostic Model for Clear Cell Renal Cell Carcinoma Based on Glycosyltransferase Gene and Verification of Key Gene Identification.International journal of molecular sciences · 2025Article
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9 authors.
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Abstract
Protein asparagine (N)-glycosylation, which promotes the folding and trafficking of cell surface receptors, has not traditionally been viewed as a viable target in oncology due to the essential and non-redundant enzymatic activities required for glycan synthesis and transfer. However, in mammals, an exception is the presence of the oligosaccharyltransferase (OST) catalytic subunit paralogs, STT3A and STT3B. In this study, we investigate the biological activity of OST inhibitors and develop a strategy for selectively inhibiting N-glycosylation that is optimized for its downstream effects on the EGFR glycoprotein. Small molecules with improved pharmacokinetic properties and selective preferences for STT3A or STT3B were synthesized, characterized in vitro, and advanced to in vivo testing. The lead compound from this series, NGI-189, induces tumor regression or growth delay in patient-derived and TKI-resistant EGFR-mutant lung cancer xenografts without causing toxicity. Collectively, these findings suggest that bioavailable OST inhibitors can be developed as therapeutic agents for oncology.
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