目的·探究后期促进复合体亚基10（anaphase-promoting complex subunit 10，ANAPC10）在肝细胞癌（liver hepatocellular carcinoma，LIHC，常简称HCC）发生发展中的生物学功能及其潜在机制。方法·通过整合癌症基因组图谱数据库（The Cancer Genome Atlas，TCGA）中LIHC（TCGA_LIHC）、中国肝癌基因组计划数据库（China Hepatocellular Carcinoma Genome Project，CHCC）乙型肝炎病毒相关亚组（hepatitis B virus related subgroup，HBV）（CHCC_HBV）及基因表达综合数据库（Gene Expression Omnibus，GEO）的数据，分析ANAPC10在HCC中的表达模式，并在HCC细胞系中采用蛋白质印迹（Western blotting）和实时荧光定量PCR（quantitative real-time PCR，q-PCR）方法验证。通过shRNA介导的基因敲低实验，在MHCC-97H和SNU-398细胞系中下调ANAPC10的表达，探究ANAPC10的敲减与HCC细胞的体外增殖能力的关系。利用小鼠高压尾静脉注射技术构建Anapc10敲除原位肝癌模型，进一步证实肝脏ANAPC10的缺失对HCC发生发展的影响。对TCGA_LIHC和CHCC_HBV的RNA测序数据进行京都基因与基因组百科全书（Kyoto Encyclopedia of Genes and Genomes，KEGG）、基因本体论（Gene Ontology，GO）通路富集分析。结果·ANAPC10在肿瘤组织中高表达，且其表达量与患者生存预后密切相关。体内外实验中下调ANAPC10可以有效抑制HCC的进展。ANAPC10主要通过影响PI3K-AKT-mTOR通路来对肿瘤的代谢进行重编程。在Anapc10敲除组的原位肝癌小鼠模型的肿瘤组织中，Akt和S6k的磷酸化水平降低；并且验证了下游脂代谢关键蛋白Fasn、Scd1的变化。结论·ANAPC10在HCC中高表达，与HCC的不良预后呈正相关，且促进HCC的发生及进展。ANAPC10激活PI3K-AKT-mTOR信号通路，促进HCC细胞的脂代谢重编程，最终促进肿瘤细胞的增殖与HCC的发生发展。

Objective ·To explore the biological functions and underlying mechanisms of anaphase-promoting complex subunit 10 (ANAPC10) in the development and progression of liver hepatocellular carcinoma (LIHC, often abbreviated as HCC). Methods ·By integrating data from The Cancer Genome Atlas (TCGA)_LIHC, the hepatitis B virus-related subgroup (HBV) of the China Hepatocellular Carcinoma Genome Project (CHCC), and the Gene Expression Omnibus (GEO), the expression pattern of ANAPC10 in HCC was analyzed. Western blotting and quantitative real-time PCR (q-PCR) were used to verify the findings in HCC cell lines. shRNA-mediated knockdown of ANAPC10 was performed in MHCC-97H and SNU-398 cell lines to investigate the effect of ANAPC10 depletion on the in vitro proliferation of HCC cells. An orthotopic liver cancer model with Anapc10 knockout was constructed using the hydrodynamic tail-vein injection technique in mice to further confirm the impact of ANAPC10 deficiency in the liver on the development and progression of HCC. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analyses were performed on the RNA-sequencing data from TCGA_LIHC and CHCC_HBV. Results ·ANAPC10 was highly expressed in tumor tissues, and its expression level was closely related to patient survival. Downregulation of ANAPC10 in vitro and in vivo effectively inhibited HCC progression. ANAPC10 mainly reprogrammed the metabolism of tumors by affecting the PI3K-AKT-mTOR pathway. In the tumor tissues of the orthotopic liver cancer mouse model in the Anapc10 knockout group, the phosphorylation levels of Akt and S6k were decreased, and changes in the key downstream lipid metabolism proteins Fasn and Scd1 were verified. Conclusion ·ANAPC10 is highly expressed in HCC and is positively correlated with poor prognosis. It promotes HCC occurrence and progression by activating the PI3K-AKT-mTOR signaling pathway and enhancing lipid metabolism reprogramming, thereby promoting tumor cell proliferation. These findings expand the understanding of ANAPC10 in tumor progression and suggest potential therapeutic targets for HCC.