Luo Y, Wang LJ, Wang CL. Mechanistic interplay between aflatoxin B1 and tissue inhibitor of metalloproteinase-3 in hepatocellular carcinoma. World J Hepatol 2025; 17(10): 109391 [DOI: 10.4254/wjh.v17.i10.109391]
Corresponding Author of This Article
Cheng-Long Wang, Department of Pathology, Chongqing Traditional Chinese Medicine Hospital, No. 6 Seventh Panxi Branch Road, Jiangbei District, Chongqing 400021, China. 171909771@qq.com
Research Domain of This Article
Gastroenterology & Hepatology
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Editorial
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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/
Oct 27, 2025 (publication date) through Oct 27, 2025
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Publication Name
World Journal of Hepatology
ISSN
1948-5182
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Luo Y, Wang LJ, Wang CL. Mechanistic interplay between aflatoxin B1 and tissue inhibitor of metalloproteinase-3 in hepatocellular carcinoma. World J Hepatol 2025; 17(10): 109391 [DOI: 10.4254/wjh.v17.i10.109391]
World J Hepatol. Oct 27, 2025; 17(10): 109391 Published online Oct 27, 2025. doi: 10.4254/wjh.v17.i10.109391
Mechanistic interplay between aflatoxin B1 and tissue inhibitor of metalloproteinase-3 in hepatocellular carcinoma
Yan Luo, Li-Juan Wang, Cheng-Long Wang
Yan Luo, Department of Stomatology, The People’s Hospital of Dadukou District, Chongqing 400084, China
Li-Juan Wang, Cheng-Long Wang, Department of Pathology, Chongqing Traditional Chinese Medicine Hospital, Chongqing 400021, China
Co-corresponding authors: Li-Juan Wang and Cheng-Long Wang.
Author contributions: Luo Y and Wang CL contributed to this paper; Wang LJ and Wang CL designed the overall concept and outline of the manuscript, contributed to the discussion, and design of the manuscript; Luo Y contributed to the writing and editing of the manuscript, and review of literature; all authors read and approved the final manuscript.
Supported by the Chongqing Health Commission and Science and Technology Bureau, No. 2023MSXM060.
Conflict-of-interest statement: All 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: Cheng-Long Wang, Department of Pathology, Chongqing Traditional Chinese Medicine Hospital, No. 6 Seventh Panxi Branch Road, Jiangbei District, Chongqing 400021, China. 171909771@qq.com
Received: May 9, 2025 Revised: June 8, 2025 Accepted: August 26, 2025 Published online: October 27, 2025 Processing time: 171 Days and 19.2 Hours
Core Tip
Core Tip: This article elucidates the critical mechanistic interplay between aflatoxin B1 (AFB1) exposure and tissue inhibitor of metalloproteinase-3 (TIMP-3) dysregulation in hepatocellular carcinoma (HCC). We propose that AFB1 contributes directly to TIMP-3 downregulation, potentially via epigenetic silencing or miRNA dysregulation, thereby promoting AFB1-related HCC aggressiveness. Understanding this AFB1-TIMP-3 axis is crucial for validating TIMP-3 as a precise prognostic biomarker and a specific therapeutic target in AFB1-related HCC. Focused research is imperative in high AFB1-exposure regions to unravel these molecular interactions and develop targeted interventions aimed at restoring TIMP-3 function, ultimately improving patient outcomes.
