The cellular response to DNA damage is crucial for maintaining the integrity and stability of molecular structure.To maintain genome stability,DNA-damaged cells should be arrested so that mutations can be repaired before replication.Although several key components required for this arrest have been discovered,the majority of the pathways are still unclear.Through a number of assays,including cell viability,colony formation,and apotheosis assay,we found that AKR1B10 protected cells from UVC-induced DNA damage.Surprisingly,UVC-induced yH2AX foci and DNA double-strand breaks in the AKR1 B10-overexpressing cells were~4-5 folds lower than those in the control group.The expression levels of AKR1B10,p53,chk1,chk2,nuclear factor(NF)-κB,and p65 showed dynamic changes in response to UVC irradiation.Our results suggested that AKR1B10 is involved in the pathway of cell cycle checkpoint and NF-κB in DNA damage.Taken together,our results suggest that AKR1B10 is involved in the repair of the DNA double-strand break,which pro-vides a new insight into the role of AKR1B10 in DNA damage repair and indicates a new trail in tumorigenesis and cancer drug resistance.