ArticleBMC cancer2024
GFPT1 accelerates immune escape in breast cancer by modifying PD-L1 via O-glycosylation.
Article in BMC cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- miR-335-3p acts as a tumor suppressor in esophageal squamous cell carcinoma and predicts favorable prognosis.Hereditas · 2026Article
- Integrated Proteomic and Metabolomic Analyses Characterise Molecular Alterations Associated with JSRV-Induced OPA.Biology · 2026Article
- Review
- Glycosylation as a dynamic regulator of RLR and cGAS-STING innate immune signalling pathways.Communications biology · 2026Review
- Metabolic reprogramming in cancer: signaling pathways and therapeutic targets.Molecular cancer · 2026Review
- O-GlcNAcylation at the tumor-immune interface: a metabolic post-translational code driving immune evasion and therapy resistance in cancer.Frontiers in immunology · 2026Review
- Editorial: Screening and discovering novel biological biomarkers by omic-data to revolutionize tumor management.Frontiers in genetics · 2025Article
- Bioinformatics insights into the role of GFPT1 in breast invasive carcinoma: implications for tumor prognosis, immune modulation, and therapeutic applications.Frontiers in genetics · 2024Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImmune escape is one of the causes of poor prognosis in breast cancer (BC). Glutamine-fructose-6-phosphate transaminase 1 (GFPT1) is the first speed-limiting enzyme of the hexosamine biosynthesis pathway (HBP) and is essential for the progression of BC. Nevertheless, the mechanism of the influence of GFPT1 in BC immune escape is not clear.
methodsFirst, the level of GFPT1 in BC was analyzed by starbase, and GFPT1 expression in BC tissues was measured by qRT-PCR, western blot and IHC. Then, the O-GlcNAc levels were detected by western blot. Thereafter, Co-IP was applied to examine the relationship between GFPT1 and PD-L1. At last, a mouse model was constructed for validation in vivo.
resultsFirstly, we discovered that GFPT1 was obviously strengthened in BC. Knockdown or introduction of GFPT1 correspondingly degraded and elevated O-GlcNAc levels in cells. Further researches revealed that there was a reciprocal relationship between GFPT1 and PD-L1. Mechanistically, we disclosed that GFPT1 enhanced PD-L1 protein stability through O-glycosylation. More interestingly, GFPT1 accelerated BC cell immune escape via upregulation of O-glycosylation-modified PD-L1. In vivo, silencing of GFPT1 attenuated immune escape of BC cells by reducing PD-L1 levels.
conclusionGFPT1 promoted BC progression and immune escape via O-glycosylation-modified PD-L1. GFPT1 may be a potential target for BC therapy.
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