ArticleFrontiers in immunology2026
Shared immune perturbations in hepatocellular carcinoma-depression comorbidity and synergistic immunotherapeutic effects of fluoxetine combined with anti-PD-1.
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
Background: Hepatocellular carcinoma (HCC) often coexists with depression, elevating patient mortality by 39%. The tryptophan metabolic axis bridges tumor and neuropsychiatric immune dysfunction, yet the immunometabolic crosstalk underlying HCC-depression comorbidity remains poorly defined, and reliable combinatorial immunotherapies are absent. Methods: We integrated public multi-omics datasets including TCGA, GEO, eQTLGen and FinnGen, and performed two-sample MR as well as genetic colocalization analyses to screen hub genes associated with HCC-depression comorbidity. GSEA/GSVA, single-cell and spatial transcriptomics were adopted to dissect gene expression and perturbed tryptophan immune pathways. In silico docking predicted fluoxetine binding to BTN3A3, GLCE and RBCK1. A Hepa1-6/CUMS comorbid mouse model combined with targeted tryptophan LC-MS metabolomics, flow cytometry and ELISA was used to verify combined therapeutic effects and tissue molecular alterations. Results: Seven overlapping risk genes for HCC and depression were identified. Conclusions: This work characterizes tryptophan-mediated immune disturbance in HCC-depression comorbidity.
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