Ma W, Baran N. Checkpoint kinase 1 as a promising target in colorectal cancer management. World J Clin Oncol 2025; 16(4): 104213 [DOI: 10.5306/wjco.v16.i4.104213]
Corresponding Author of This Article
Wenxue Ma, MD, PhD, Professor, Department of Medicine, Sanford Stem Cell Institute, Moores Cancer Center, University of California San Diego, 2880 Torrey Pines Scenic Drive, MC 0695, La Jolla, CA 92093, United States. wma@health.ucsd.edu
Research Domain of This Article
Oncology
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Clin Oncol. Apr 24, 2025; 16(4): 104213 Published online Apr 24, 2025. doi: 10.5306/wjco.v16.i4.104213
Checkpoint kinase 1 as a promising target in colorectal cancer management
Wenxue Ma, Natalia Baran
Wenxue Ma, Department of Medicine, Sanford Stem Cell Institute, Moores Cancer Center, University of California San Diego, La Jolla, CA 92093, United States
Natalia Baran, Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, United States
Natalia Baran, Department of Experimental Hematology, Institute of Hematology and Transfusion Medicine, Warsaw 00-791, Mazowieckie, Poland
Author contributions: Ma W reviewed the relevant literature, designed the concept and outline of this editorial, wrote, edited, and finalized the manuscript for publication; Baran N reviewed and provided critical review and edits to enhance the content.
Conflict-of-interest statement: The authors report no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Wenxue Ma, MD, PhD, Professor, Department of Medicine, Sanford Stem Cell Institute, Moores Cancer Center, University of California San Diego, 2880 Torrey Pines Scenic Drive, MC 0695, La Jolla, CA 92093, United States. wma@health.ucsd.edu
Received: December 16, 2024 Revised: January 14, 2025 Accepted: January 15, 2025 Published online: April 24, 2025 Processing time: 103 Days and 6.4 Hours
Abstract
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.
