Published online Apr 24, 2025. doi: 10.5306/wjco.v16.i4.104213
Revised: January 14, 2025
Accepted: January 15, 2025
Published online: April 24, 2025
Processing time: 103 Days and 6.4 Hours
This editorial provides insights into the pivotal role of checkpoint kinase 1 (CHEK1) as both a biomarker and therapeutic target in colorectal cancer (CRC), based on findings from a recent study by Pang et al. Using single-cell RNA sequencing and immunohistochemistry, the study demonstrates significant CHEK1 overexpression in CRC tissues and identifies nitidine chloride as a potent CHEK1 inhibitor that disrupts DNA damage repair pathways. These findings underscore the therapeutic potential of CHEK1 inhibition and highlight the need for further research to address gaps in CRC treatment.
Core Tip: This editorial highlights checkpoint kinase 1 (CHEK1) as a novel biomarker and therapeutic target in colorectal cancer (CRC). Pang et al demonstrate significant CHEK1 overexpression in CRC tissues using single-cell RNA sequencing, immunohistochemistry, and tissue microarray analyses. They identify nitidine chloride as a potent CHEK1 inhibitor that disrupts DNA damage repair, impairing tumor progression. These findings emphasize CHEK1's potential for improving CRC diagnosis and treatment while addressing research needs for clinical validation and tumor microenvironment exploration.
