ReviewClinical and translational medicine2026
Regulatory mechanism of O-linked N-acetylglucosamine protein modification on autophagy in cancer.
Review in Clinical and translational medicine, 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.
The trial behind it
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Who cites it
1 citing paper in PubMed.
- Regulatory mechanism of O-linked N-acetylglucosamine protein modification on autophagy in cancer.Clinical and translational medicine · 2026Review
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6 authors.
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Abstract
backgroundO-linked N-acetylglucosamine protein modification (O-GlcNAcylation) is a dynamic, nutrient-sensitive post-translational modification frequently upregulated in cancers. Autophagy, a lysosome-dependent recycling pathway, plays a context-dependent dual role in tumorigenesis and therapy resistance. Emerging evidence reveals intricate crosstalk between these two processes, positioning the O-GlcNAcylation-autophagy axis as a critical regulator of cancer cell adaptation. MAIN TOPICS: This review systematically delineates the multidimensional mechanisms by which O-GlcNAcylation regulates distinct stages of autophagy initiation, maturation, and fusion across various cancer types. We detail how O-GlcNAcylation targets core autophagy machinery, including the ULK1 complex, LC3 lipidation system, and SNARE fusion proteins, and modulates key signaling hubs like mTOR and AMPK. Furthermore, we integrate this molecular regulation with the stage-specific pro-tumor or tumor-suppressive functions of autophagy, highlighting how O-GlcNAcylation remodels autophagic flux to promote metabolic reprogramming, stress survival, and therapeutic resistance.
conclusionsThe O-GlcNAcylation-autophagy axis represents a promising therapeutic target. Combining small-molecule inhibitors of O-GlcNAc cycling enzymes (OGT/OGA) with autophagy modulators offers a novel strategy to overcome tumor drug resistance. Future research must address the heterogeneity of this regulatory network across cancer types and developmental stages to advance precision oncology interventions. KEYPOINTS: O-GlcNAcylation serves as a nutrient and stress sensor that dynamically regulates autophagy at multiple stages in cancer cells. It fine-tunes autophagy initiation, maturation and fusion by modifying key proteins such as ULK1, ATG4B and SNAP-29. Context-dependent O-GlcNAcylation promotes tumour adaptation and therapy resistance via autophagy remodelling. Targeting the O-GlcNAc-autophagy axis offers a promising strategy to overcome cancer drug resistance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.