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25 reviewsRecent evidence has highlighted immune checkpoint inhibitors as among the most promising immunotherapies for variousmalignancies. However, a significant proportion of HCC patients exhibit poor responses. Lipid metabolic heterogeneity isconsidered a key driver of cancer progression. However, the role of lipid metabolic reprogramming in HCC immunotherapyresistance remains poorly understood. Herein, we aimed to illuminate the potential relationship between lipid metabolicreprogramming and ICI resistance and provide novel strategies to increase the HCC immunotherapy response. Patients whoreceived PD-1/PD-L1 inhibitors were enrolled. The effect of TACC3 on the tumor microenvironment was validated via single-cellRNA sequencing in HCC-bearing mouse models. Targeted metabolomics was performed to analyze the regulatory role of TACC3 in1234567890();,:HCC metabolism. To address HCC immunotherapy resistance, we developed a targeted nucleic acid therapeutic utilizingN-acetylgalactosamine (GalNAc) to conjugate siTACC3. Through clinical cohort analysis, we found that TACC3 was overexpressed inHCC patients with poor response to immunotherapy. Furthermore, we demonstrated that silencing tumor-derived TACC3 optimizesthe cytotoxicity of infiltrating CD8+ T lymphocytes. Both in vitro and in vivo assays suggested that TACC3 maintains ACSL4-mediated polyunsaturated fatty acid (PUFA) metabolism in HCC cells. Additionally, TACC3 accelerates ACSL4 expression byinteracting with LARP1 and PABPC1, which stabilize ACSL4 mRNA. The results of preclinical models demonstrated the satisfactoryefficacy of GalNAc-conjugated siTACC3 combined with PD-1 inhibitor therapy for HCC. In summary, tumor-derived TACC3 impairsthe tumor-killing activity of CD8+ T lymphocytes through PUFA metabolism-associated crosstalk. Targeting TACC3 represents anovel and practicable strategy to augment ICI efficacy against HCC.Signal Transduction and
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