Ren LN, Liu C, Jin CQ, Zhang XH. From association to intervention: Rethinking CD24’s causal role in hepatocellular carcinogenesis. World J Gastrointest Oncol 2026; 18(6): 117434 [DOI: 10.4251/wjgo.v18.i6.117434]
Corresponding Author of This Article
Cheng-Qiang Jin, Director, Department of Laboratory Medicine, Affiliated Hospital of Jining Medical University, No. 89 Guhuai Road, Jining 272029, Shandong Province, China. jincq2008@163.com
Research Domain of This Article
Chemistry, Organic
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review-article
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Ren LN, Liu C, Jin CQ, Zhang XH. From association to intervention: Rethinking CD24’s causal role in hepatocellular carcinogenesis. World J Gastrointest Oncol 2026; 18(6): 117434 [DOI: 10.4251/wjgo.v18.i6.117434]
Li-Na Ren, Cheng-Qiang Jin, Xiang-Hui Zhang, Department of Laboratory Medicine, Affiliated Hospital of Jining Medical University, Jining 272029, Shandong Province, China
Cong Liu, College of Medical Imaging and Laboratory, Jining Medical University, Jining 272067, Shandong Province, China
Co-first authors: Li-Na Ren and Cong Liu.
Co-corresponding authors: Cheng-Qiang Jin and Xiang-Hui Zhang.
Author contributions: Ren LN designed the article, analyzed the data, and drafted the manuscript; Jin CQ and Zhang XH provided joint supervision and analyzed clinical data. they contributed equally to this article, they are the co-corresponding authors of this manuscript; All authors have read and approved the final manuscript. Jin CQ and Zhang XH contributed equally to this article and are the co-corresponding authors of this manuscript. Ren LN and Liu C contributed equally to this article and are the co-first authors of this manuscript.
AI contribution statement: We used an AI-based tool (Kimi) solely for language editing to improve the clarity and readability of the English. The manuscript was written entirely by the authors. No part of the academic content or scholarly interpretation was generated by AI. All figures and graphical elements were created by the authors without the use of AI-generated tools. The conceptual framework, argumentation, and conclusions are entirely the result of the authors’ own scholarly work.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
Corresponding author: Cheng-Qiang Jin, Director, Department of Laboratory Medicine, Affiliated Hospital of Jining Medical University, No. 89 Guhuai Road, Jining 272029, Shandong Province, China. jincq2008@163.com
Received: December 8, 2025 Revised: February 12, 2026 Accepted: April 1, 2026 Published online: June 15, 2026 Processing time: 184 Days and 18.7 Hours
Abstract
Recent longitudinal studies have demonstrated progressive upregulation of cluster of differentiation 24 (CD24) during hepatocarcinogenesis, correlating with programmed death-ligand 1 (PD-L1) expression and enhancing detection of alpha-fetoprotein-negative hepatocellular carcinoma by approximately 20%. Circulating CD24+ T cells show expansion patterns that could track minimal residual disease. Yet this evidence is largely observational, with gaps in functional validation, subset-specific analysis, and mechanistic links to PD-L1 transcription. Spatial mapping, survival data, and isoform distinctions remain unexplored. To establish CD24 as a bona fide therapeutic target rather than merely a correlative marker, future investigations must employ clustered regularly interspaced short palindromic repeats-based functional genomics, single-cell multi-omics integration, spatial transcriptomics, and isoform-discriminating soluble CD24 assays to definitively demonstrate causality and clinical utility.
Core Tip: While cluster of differentiation 24 (CD24) is dynamically upregulated during hepatocarcinogenesis and improves the detection of alpha-fetoprotein-negative hepatocellular carcinoma, it currently lacks functional validation, resolution of specific subsets, and a clear mechanistic linkage to programmed death-ligand 1. Functional genetics, single-cell, multi-omics, and spatial analyses are needed to confirm CD24’s causality and therapeutic potential.
