ArticleJournal of experimental & clinical cancer research : CR2023
B4GALT1 promotes immune escape by regulating the expression of PD-L1 at multiple levels in lung adenocarcinoma.
Article in Journal of experimental & clinical cancer research : CR, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed.
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- Optimized Simultaneous N/O-Glycopeptide Enrichment Strategy Identifies Lung Cancer Diagnostic Biomarkers in Serum.Journal of proteome research · 2026Article
- JAK-STAT signaling pathway in cancer: from molecular mechanisms to clinical intervention.Molecular cancer · 2026Review
- TRIM28-mediated SUMOylation of SREBF1 drives PD‑L1 N‑glycosylation and immune evasion in bladder cancer.Cell death & disease · 2026Article
- Multi-omics analysis identified serumJournal of thoracic disease · 2026Article
- Integrated single-cell and bulk RNA sequencing reveals novel biomarkers of invasive adenocarcinoma subtypes in lung adenocarcinoma.Translational cancer research · 2026Article
- PFDN5 synergizes with anti-PD1 therapy to promote triple-negative breast cancer cell death through JAK2/STAT3/c-Myc signaling axis.Journal of translational medicine · 2026Article
- B4GALT1 deficiency attenuates steatohepatitis by regulating the PPARγ/ACSL4 axis.Hepatology communications · 2026Article
- B4GALNT4-Mediated Glycosylation of PDK1 Activates the PI3K-AKT Signaling Pathway to Promote Prostate Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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- A risk score model based on glycosylation-related genes for predicting radioresistance and prognosis of lung adenocarcinoma.Translational cancer research · 2026Article
- DCLK1 drives malignant progression and chemoresistance of bladder cancer by deubiquitinating HDAC6.Molecular cancer · 2026Article
- Post-translational modifications of immune checkpoints: molecular mechanisms, tumor microenvironment remodeling, and therapeutic implications.Journal of biomedical science · 2026Review
- SIRT2 is associated with prognosis, ferroptosis susceptibility, and immune infiltration in lung adenocarcinoma.Frontiers in oncology · 2026Article
- LAMP5 as a novel prognostic biomarker linked to the tumor immune microenvironment in esophageal squamous cell carcinoma.American journal of cancer research · 2026Article
- Mediterranean diet adherence is associated with antiviral, neuroimmune, and cardiometabolic proteomic profiles in people with HIV.Frontiers in nutrition · 2026Article
- Regulation of glycosylation in radiotherapy: exploring the multiple effects of DNA damage, immune response, stromal microenvironment and metabolism.Frontiers in oncology · 2026Review
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- Global proteomic analysis ofmSystems · 2025Article
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9 authors.
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Abstract
backgroundInvasive adenocarcinoma (IAC), which is typically preceded by minimally invasive adenocarcinoma (MIA), is the dominant pathological subtype of early-stage lung adenocarcinoma (LUAD). Identifying the molecular events underlying the progression from MIA to IAC may provide a crucial perspective and boost the exploration of novel strategies for early-stage LUAD diagnosis and treatment.
methodsTranscriptome sequencing of four pairs of MIA and IAC tumours obtained from four multiple primary lung cancer patients was performed to screen out beta-1,4-galactosyltransferase1 (B4GALT1). Function and mechanism experiments in vitro and in vivo were performed to explore the regulatory mechanism of B4GALT1-mediated immune evasion by regulating programmed cell death ligand 1 (PD-L1).
resultsB4GALT1, a key gene involved in N-glycan biosynthesis, was highly expressed in IAC samples. Further experiments revealed that B4GALT1 regulated LUAD cell proliferation and invasion both in vitro and in vivo and was related to the impaired antitumour capacity of CD8 + T cells. Mechanistically, B4GALT1 directly mediates the N-linked glycosylation of PD-L1 protein, thus preventing PD-L1 degradation at the posttranscriptional level. In addition, B4GALT1 stabilized the TAZ protein via glycosylation, which activated CD274 at the transcriptional level. These factors lead to lung cancer immune escape. Importantly, inhibition of B4GALT1 increased CD8 + T-cell abundance and activity and enhanced the antitumour immunity of anti-PD-1 therapy in vivo.
conclusionB4GALT1 is a critical molecule in the development of early-stage LUAD and may be a novel target for LUAD intervention and immunotherapy.
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