ArticleFrontiers in immunology2026
D-xylose suppresses hepatocellular carcinoma progression by regulating dihydrodiol dehydrogenase and remodeling the immune microenvironment.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death with limited treatment options. Dihydrodiol dehydrogenase (DHDH), an enzyme involved in D-xylose metabolism, has unclear roles in tumorigenesis and immune regulation. This study aims to investigate the clinical significance, biological functions, and immunomodulatory mechanisms of DHDH in HCC, and to explore the therapeutic potential of targeting its metabolic activity. Methods: DHDH expression and its clinical correlation were analyzed using TCGA-LIHC data and validated in HCC tissue microarrays. Results: DHDH was highly expressed in HCC tissues and significantly associated with poor prognosis. Functional studies demonstrated that DHDH overexpression promoted HCC cell proliferation and invasion while suppressing CD8 Discussion: DHDH drives HCC progression and immune evasion by promoting an immunosuppressive microenvironment. Targeting DHDH with D-xylose restores CD8
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