ArticleFrontiers in oncology2022
TGF-β1-Mediated PD-L1 Glycosylation Contributes to Immune Escape
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 20 citations in OpenAlex.
- Potential of RAD51C as a hub gene and therapeutic target in bladder cancer: insights from bioinformatics and experimental analysis.International journal of surgery (London, England) · 2026Article
- C1ORF112 drives lung adenocarcinoma progression through e2f8-mediated transcriptional activation.Journal of thoracic disease · 2026Article
- Core regulatory mechanisms of the PD-L1 axis and clinical strategies for immune escape and immunotherapy response in nasopharyngeal carcinoma.Translational oncology · 2026Review
- Research progress on the mechanisms of EB virus reshaping the immune microenvironment in nasopharyngeal carcinoma.Clinical and experimental medicine · 2026Review
- Article
- Post-translational modifications of immune checkpoints: molecular mechanisms, tumor microenvironment remodeling, and therapeutic implications.Journal of biomedical science · 2026Review
- Proteomics Combined with N-Glycoproteomics to Explore the Pathogenesis of Nasopharyngeal Carcinoma.Journal of proteome research · 2025Article
- Targeting DDOST improves the efficacy of lenvatinib and immunotherapy in hepatocellular carcinoma.Experimental & molecular medicine · 2025Article
- Integrated multi-omics analysis identifies key biomarkers associated with post-translational modifications and RNA methylation in clear cell renal cell carcinoma.Discover oncology · 2025Article
- The mechanism and research progress of PD-1/PD-L1 on immune escape of lung cancer.Translational cancer research · 2025Review
- Exosomal PD-L1 derived from hypoxia nasopharyngeal carcinoma cell exacerbates CD8Cancer immunology, immunotherapy : CII · 2025Article
- Jun, an Oncological Foe or Friend?International journal of molecular sciences · 2025Review
- Altered glycosylation in cancer: molecular functions and therapeutic potential.Cancer communications (London, England) · 2024Review
- Regulation of post-translational modification of PD-L1 and associated opportunities for novel small-molecule therapeutics.Future medicinal chemistry · 2024Review
- Glycosylation in the tumor immune response: the bitter side of sweetness.Acta biochimica et biophysica Sinica · 2024Review
- Emerging therapeutic frontiers in cancer: insights into posttranslational modifications of PD-1/PD-L1 and regulatory pathways.Experimental hematology & oncology · 2024Review
- Nasopharyngeal carcinoma: current views on the tumor microenvironment's impact on drug resistance and clinical outcomes.Molecular cancer · 2024Review
- Review
- Glycosylation Targeting: A Paradigm Shift in Cancer Immunotherapy.International journal of biological sciences · 2024Review
- PTMs of PD-1/PD-L1 and PROTACs application for improving cancer immunotherapy.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunotherapy targeting programmed death ligand-1/programmed cell death protein-1 (PD-L1/PD-1) has achieved great success in multiple cancers, but only a small subset of patients showed clinical responses. Recent evidences have shown that post-translational modification of PD-L1 protein could regulate its protein stability and interaction with cognate receptor PD-1, thereby affecting anticancer immunotherapy in several solid tumors. However, the molecular mechanisms underlying how PD-1/PD-L1 expression is regulated still remain unclear in nasopharyngeal carcinoma (NPC). Here, we found N-glycosylation of PD-L1 in NPC cells and tissues. Mechanistically, we showed that STT3A transferred N-linked glycans to PD-L1, and TGF-β1 could positively regulate STT3A expression through activating c-Jun to bind to STT3A promoter. Functional assays showed that inhibition of TGF-β1 resulted in a decrease of glycosylated PD-L1 and enhanced cytotoxic T-cell function against NPC cells. Analysis of clinical specimens revealed that the expression of STT3A was positively correlated with TGF-β1 and c-Jun, and high STT3A expression was positively correlated with a more advanced clinical stage. Altogether, TGF-β1 activated c-Jun/STT3A signaling pathway to promote N-glycosylation of PD-L1, thus further facilitating immune evasion and reducing the efficacy of cancer immunotherapy. As such, all these data suggested that targeting TGF-β1 pathway might be a promising approach to enhance immune checkpoint blockade, and simultaneous blockade of PD-L1 and TGF-β1 pathways might elicit potent and superior antitumor activity relative to monotherapies.
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