Xu M, Ruan TT, Tang H, Fang RF, Sai WL, Xie Q, Yao DF, Yao M. Up-regulated programmed cell death protein-1/its ligand 1 expression promotes metabolic dysfunction-associated steatotic liver disease malignant progression. World J Gastrointest Oncol 2025; 17(5): 104842 [DOI: 10.4251/wjgo.v17.i5.104842]
Corresponding Author of This Article
Deng-Fu Yao, MD, Doctor, Department of Immunology, Medical School of Nantong University and Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, No. 20 West Temple Road, Nantong 226001, Jiangsu Province, China. yaodf@ahnmc.com
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/
Min Xu, Tian-Tian Ruan, Hao Tang, Rong-Fei Fang, Wen-Li Sai, Qun Xie, Deng-Fu Yao, Min Yao
Min Xu, Tian-Tian Ruan, Hao Tang, Wen-Li Sai, Deng-Fu Yao, Min Yao, Department of Immunology, Medical School of Nantong University and Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
Rong-Fei Fang, Department of Gastroenterology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
Qun Xie, Department of Infectious Diseases, Nantong Haian People’s Hospital, Haian 226600, Jiangsu Province, China
Co-first authors: Min Xu and Tian-Tian Ruan.
Co-corresponding authors: Min Yao and Deng-Fu Yao.
Author contributions: Xu M, Ruan TT and Tang H contributed equally to this work and wrote draft of the paper; Fang RF, Sai WL and Xie Q performed literature search for the manuscript; Yao M and Yao DF revised the manuscript and edited all drafts of the paper; All authors approved the final version of the manuscript.
Supported by National Natural Science Foundation of China, No. 81673241 and No. 32470985.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
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: Deng-Fu Yao, MD, Doctor, Department of Immunology, Medical School of Nantong University and Research Center of Clinical Medicine, Affiliated Hospital of Nantong University, No. 20 West Temple Road, Nantong 226001, Jiangsu Province, China. yaodf@ahnmc.com
Received: January 6, 2025 Revised: March 20, 2025 Accepted: April 1, 2025 Published online: May 15, 2025 Processing time: 131 Days and 23.8 Hours
Abstract
This editorial focuses on the recent article by Yang et al in the World Journal of Gastrointestinal Oncology, which highlights the role of interlukin-17A in promoting hepatocellular carcinoma (HCC) progression by up-regulated programmed cell death protein-1 (PD-1)/programmed cell death protein ligand-1 (PD-L1) expression. Previous, the high PD-1/PD-L1 level was due to hepatitis virus infection leading to systemic innate immune tolerance and cluster of differentiation 8 + T cells exhaustion, ultimately leading to HCC. Recently, interesting studies have found that the malignant progression of metabolic dysfunction-associated steatotic/fatty liver disease (MASLD/MAFLD), that is former nonalcoholic fatty liver disease, was achieved by up-regulated PD-L1 level that was activated the cGAS-STING pathway under lipid accumulation with mitochondrial DNA overflow and up-regulated PD-1/PD-L1 to promote MASLD malignant transformation via immune escape. These data suggested that PD-1 or PD-L1 should be a promising target for preventing or delaying non-viral liver disease malignant progression except of antiviral therapy for HCC.
Core Tip: Hepatocellular carcinoma (HCC) is associated with hepatitis virus (hepatitis B virus or hepatitis C virus) infection and increasing metabolic dysfunction-associated steatotic/fatty liver disease (MASLD/MAFLD). Virus vaccines and antiviral therapy are considered key prevention and anti-viral treatments for HCC. Recently, interesting observation was that MASLD malignant progression was associated with higher programmed cell death protein-1/its ligand 1 (PD-1/PD-L1) expression. Therefore, inhibiting PD-1/PD-L1 except of HCC therapy could be a promising target to prevent or delay the malignant transformation of hepatocytes.
