Objective The DNA repair-related protein RAD23B has been implicated in the progression of various malignancies. This study aimed to investigate the role of RAD23B in promoting colorectal cancer ( CRC) metastasis and to elucidate the underlying molecular mechanisms. Methods Cell proliferation, migration, and invasion were assessed using Cell Counting Kit-8 and Transwell assays. A xenograft mouse model was used to evaluate the metastatic potential in vivo. Transcriptomic analysis was carried out by RNA sequencing (RNA-seq) to identify signaling pathways regulated by RAD23B. Expression levels of RAD23B, Talin1, Integrinαv, Integrinβ1, phosphoinositide 3-kinase ( PI3K), phosphorylated PI3K, protein kinase B ( AKT), phosphorylated AKT, and matrix metalloproteinase 9 (MMP9) were measured by Western blot. Results In vitro, overexpression of RAD23B significantly enhanced the proliferation, migration, and invasion abilities of colorectal cancer SW480 and HCT-8 cells (P<0. 05). In the in vivo model, RAD23B overexpression notably increased the number of liver metastatic foci in mice(P<0. 05), indicating that RAD23B promotes the liver metastasis potential of colorectal cancer cells. RNA sequencing revealed that RAD23B overexpression activated cell adhesion, integrin, and PI3K-AKT signaling pathways in SW480 cells ( P<0. 05 ). Western blot analysis demonstrated that RAD23B overexpression upregulated the expression of Talin1, Integrinαv, Integrinβ1, p-PI3K, PI3K, p-AKT, AKT, and MMP9(P<0. 05). Conclusions RAD23B promotes CRC liver metastasis through activation of the Talin1 / Integrin / PI3K/ AKT / MMP9 axis.