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.

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.