【摘要】 目的 裂解和多腺苷酸化特异性因子3(CPSF3)在肝细胞癌(LIHC)及泛癌中的表达特征、预后价值及其在肿瘤免疫调控和细胞增殖中的作用。方法 基于公开数据库对CPSF3的表达水平、预后意义及其与肿瘤免疫细胞浸润的关系进行系统分析；结合体外细胞实验和体内动物模型，验证CPSF3对肿瘤细胞增殖及免疫抑制性细胞浸润的调控作用。结果 CPSF3在多种肿瘤组织中呈高表达状态，且与患者不良预后显著相关。功能分析显示，CPSF3可能通过调控细胞周期相关信号通路促进肿瘤细胞增殖。实验结果进一步表明，抑制CPSF3表达可显著抑制LIHC细胞增殖，并减少肿瘤组织中髓源性抑制细胞(MDSCs)的浸润。结论 CPSF3在肿瘤进展中发挥促癌作用，其高表达与免疫抑制微环境形成及不良预后密切相关，可能成为LIHC等肿瘤的潜在预后标志物及免疫治疗靶点。更多还原

【Abstract】 Objective To investigate the expression profile, prognostic value, and immunoregulatory role of cleavage and polyadenylation specific factor 3(CPSF3) in liver hepatocellular carcinoma(LIHC) and pan-cancer, as well as its function in tumor immune regulation and cell proliferation. Methods Publicly available datasets were analyzed to evaluate CPSF3 expression, its prognostic value, and its association with tumor immune cell infiltration. In addition, in vitro cell experiments and in vivo animal models were employed to validate the regulatory effects of CPSF3 on tumor cell proliferation and immunosuppressive cell infiltration. Results CPSF3 exhibited high expression levels in various tumor tissues and was significantly associated with poor prognosis in patients. Functional analysis revealed that CPSF3 might promote tumor cell proliferation by regulating cell cycle-related signaling pathways. Experimental results further demonstrated that inhibiting CPSF3 expression significantly suppressed LIHC cell proliferation and reduced the infiltration of myeloid-derived suppressor cells(MDSCs) in tumor tissues. Conclusion CPSF3 exerts a pro-tumorigenic role in tumor progression. Its high expression is closely associated with the formation of an immunosuppressive tumor microenvironment and poor prognosis, suggesting that it may serve as a potential prognostic biomarker and immunotherapeutic target for tumors such as LIHC.更多还原