Rad54l-KO Mouse

Rad54l, a DNA motor protein, is a key member of the SWI2/SNF2 protein family. It plays multiple roles in homologous recombination DNA repair (HR), such as catalyzing the reversal and restoration of model replication forks in vitro. It is involved in regulating DNA replication dynamics, and the homologous recombination repair pathway is crucial for maintaining genome stability [2,3,4,5,6,7].

In cancer research, high Rad54l expression in bladder cancer tissue is associated with poor prognosis, promoting abnormal cell proliferation by regulating the cell cycle and senescence, and may be associated with p53, p21, and pRB [1]. In hepatocellular carcinoma, its up-regulation is positively correlated with tumor pathological staging and negatively associated with patient overall survival, and it is correlated with Edmondson-Steiner grade and the proliferation-related gene Ki67 [3]. In early-stage lung adenocarcinoma, high expression of Rad54l is related to worse overall survival, and it is an independent prognostic factor [6]. Also, in pan-cancer analysis, Rad54l is highly expressed in most tumors, associated with survival outcomes, immune cell infiltration, TMB, MSI, and immune checkpoints, and promotes the proliferation and migration of HCC cells in vitro [7].

In conclusion, Rad54l is essential for homologous recombination DNA repair and regulating DNA replication. Its dysregulation is closely associated with the progression of various cancers including bladder, liver, and lung adenocarcinoma. Understanding Rad54l's function through research can provide potential prognostic biomarkers and treatment targets for these cancers.