biostudies-literatureUnknown13(2)Li CColorectal cancer (CRC) poses a significant global health challenge, with liver metastasis being a major contributor to its high mortality rate. The liver, due to its strategic anatomical location, distinctive tissue architecture, and unique metabolic properties, is the primary site for CRC to metastasize. The objective of this study was to identify hub genes involved in colorectal liver metastasis (CRLM) using a combination of bioinformatics analysis and experimental methods, and to decipher their molecular mechanisms that regulate this metastatic process. By mining data from the TCGA and GEO databases, we identified that low expression of 3-ketoacid CoA transferase 1 (OXCT1) might related to the development of CRLM. Both <i>in vitro</i> and <i>in vivo</i> experiments have indicated that Genes & diseases101625https://www.ebi.ac.uk/biostudies/studies/S-EPMC12765264biostudies-literatureLow expression of OXCT1 promote colorectal cancer liver metastasis by upregulating CDK8 and β-catenin via H3 acetylation.PMC12765264Wu KGong DYang JShan XLi CHuang YTang NZhu YZhang RWang KfalseLow expression of OXCT1 promote colorectal cancer liver metastasis by upregulating CDK8 and β-catenin via H3 acetylation.Colorectal cancer (CRC) poses a significant global health challenge, with liver metastasis being a major contributor to its high mortality rate. The liver, due to its strategic anatomical location, distinctive tissue architecture, and unique metabolic properties, is the primary site for CRC to metastasize. The objective of this study was to identify hub genes involved in colorectal liver metastasis (CRLM) using a combination of bioinformatics analysis and experimental methods, and to decipher their molecular mechanisms that regulate this metastatic process. By mining data from the TCGA and GEO databases, we identified that low expression of 3-ketoacid CoA transferase 1 (OXCT1) might related to the development of CRLM. Both <i>in vitro</i> and <i>in vivo</i> experiments have indicated that 2026-01-01T00:00:00Z2026 Mar2026-06-17T04:46:35.02Z2026-06-17T03:06:57.439ZS-EPMC127652644149247010.1016/j.gendis.2025.101625