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Identifying novel drivers of immune evasion is crucial for improving therapeutic strategies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We employed a multi-omics integrative framework to identify HCC-specific immune biomarkers. Functional roles were validated using in vitro and in vivo models, including UDP-glucuronate decarboxylase 1 (UXS1) knockout\/overexpression, co-culture assays, and various mouse models. Molecular mechanisms were dissected using immunoprecipitation coupled with mass spectrometry, ubiquitination assays, chromatin immunoprecipitation, luciferase reporter assays, and single-cell RNA sequencing.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We identified the glycosyltransferase UXS1 as a novel immune-related prognostic hub gene in HCC. UXS1 was upregulated due to copy number gain and MZF1-driven promoter hypomethylation. Functionally, UXS1 promoted HCC malignancy independently of its canonical enzymatic activity. Mechanistically, UXS1 interacted with the E3 ligase F-box and WD repeat domain-containing 7 (FBXW7) to promote histone-lysine N-methyltransferase 2D (KMT2D) ubiquitination and degradation. We further discovered that KMT2D, acting as a non-catalytic scaffold, recruited the transcriptional repressor CCAAT enhancer binding protein beta (CEBPB) to the PD-L1 promoter to maintain its repression. UXS1-mediated KMT2D degradation disrupted this complex, leading to CEBPB dissociation and consequent PD-L1 transcriptional derepression. In vivo, UXS1 suppressed CD8\n                      <jats:sup>+<\/jats:sup>\n                      T-cell effector function. UXS1 knockout synergized with anti-PD-1 therapy, and in human HCC, high UXS1 correlated with low KMT2D, high PD-L1, and reduced CD8\n                      <jats:sup>+<\/jats:sup>\n                      T-cell infiltration.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This study defines a novel UXS1-KMT2D-CEBPB-PD-L1 signaling axis, revealing how UXS1 drives immune evasion in HCC via epigenetic reprogramming. Targeting this axis may represent a potential strategy to overcome immune resistance, warranting further clinical investigation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jitc-2025-013948","type":"journal-article","created":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T13:45:31Z","timestamp":1783518331000},"page":"e013948","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["UDP-glucuronate decarboxylase 1 promotes tumor immune evasion by accelerating KMT2D loss in hepatocellular carcinoma"],"prefix":"10.1136","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8912-5069","authenticated-orcid":false,"given":"Jiwei","family":"Zhang","sequence":"first","affiliation":[{"name":"The MOE Key Laboratory for Standardization of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China"},{"name":"State Key Laboratory of Discovery 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