CHEK1, also known as checkpoint kinase 1, is a key signal transducer inside the genomic integrity checkpoints. It is involved in the cell cycle checkpoint pathways, responding to DNA damage. When DNA is under stress from endogenous or exogenous damaging agents, the cell activates the ATM-Chk2 and ATR-Chk1 pathways, with CHEK1 being a downstream effector in the ATR-Chk1 pathway. This pathway is crucial for the cell to either halt the cell cycle or initiate apoptosis in response to DNA damage, ensuring genome stability [4,5].

CHEK1 is overexpressed in a range of cancers such as lung adenocarcinoma, multiple myeloma, and is associated with TP53 mutations in lung tumors. In lung adenocarcinoma, its overexpression, potentially triggered by promoter methylation, amplification, and miRNA regulation, signals a poor prognosis. In multiple myeloma, high CHEK1 expression is linked to poor outcomes, and it promotes cellular proliferation, drug-resistance, chromosomal instability, and osteoclast differentiation. In lung squamous carcinoma, miR-139-3p can target CHEK1, modulating DNA repair and cell viability. Also, in diabetic nephropathy, CHEK1 may be a biomarker of glomerular epithelial cell injury [1,2,3,6,7,8].

In conclusion, CHEK1 is essential for maintaining genomic integrity through its role in the DNA damage response and cell cycle regulation. Its dysregulation is associated with various cancers and other diseases, highlighting its potential as a biomarker and therapeutic target. Studies on CHEK1 in different disease models have provided insights into its functions in disease development, which could be valuable for future treatment strategies.