Xiao FK, Li P, Li XM, Mi Y. MEX3A promotes hepatocellular carcinoma cell proliferation and migration via the Wnt/β-catenin and EMT pathways. World J Gastrointest Oncol 2025; 17(10): 106410 [PMID: 41114094 DOI: 10.4251/wjgo.v17.i10.106410]
Corresponding Author of This Article
Fan-Kai Xiao, MD, PhD, Associate Professor, Department of Oncology, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe Road, Zhengzhou 450052, Henan Province, China. xfkw@hotmail.com
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Oncology
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Letter to the Editor
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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 15, 2025 (publication date) through Oct 26, 2025
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World Journal of Gastrointestinal Oncology
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1948-5204
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Xiao FK, Li P, Li XM, Mi Y. MEX3A promotes hepatocellular carcinoma cell proliferation and migration via the Wnt/β-catenin and EMT pathways. World J Gastrointest Oncol 2025; 17(10): 106410 [PMID: 41114094 DOI: 10.4251/wjgo.v17.i10.106410]
World J Gastrointest Oncol. Oct 15, 2025; 17(10): 106410 Published online Oct 15, 2025. doi: 10.4251/wjgo.v17.i10.106410
MEX3A promotes hepatocellular carcinoma cell proliferation and migration via the Wnt/β-catenin and EMT pathways
Fan-Kai Xiao, Ping Li, Xin-Min Li, Yin Mi
Fan-Kai Xiao, Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China
Ping Li, Department of Medical, Henan Medical College, Zhengzhou 451191, Henan Province, China
Xin-Min Li, Department of Pathology, Women and Infants Hospital of Zhengzhou, Zhengzhou 450052, Henan Province, China
Yin Mi, Department of Radiation Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China
Author contributions: Xiao FK designed the overall concept and outline of the manuscript; Xiao FK, Li P, Li XM and Mi Y contributed to the writing and editing of the manuscript; all authors have read and approved the final manuscript.
Supported by Youth Foundation of Henan Scientific Committee, No. 202300410416; and Henan Province Medical Science, Technology Breakthrough Plan Project, No. LHGJ20190033.
Conflict-of-interest statement: The authors report no conflicts 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: Fan-Kai Xiao, MD, PhD, Associate Professor, Department of Oncology, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe Road, Zhengzhou 450052, Henan Province, China. xfkw@hotmail.com
Received: February 26, 2025 Revised: April 29, 2025 Accepted: June 16, 2025 Published online: October 15, 2025 Processing time: 231 Days and 3.6 Hours
Abstract
In this paper, we focus on compelling evidence showing that MEX3A is significantly overexpressed in hepatocellular carcinoma (HCC) and correlates with poor prognosis. A recent study by Ji et al highlights MEX3A’s role in driving proliferation and migration via the RORA/β-catenin axis and epithelial-mesenchymal transition, positioning it as a potential biomarker and therapeutic target. This study addresses a critical gap in understanding HCC pathogenesis and offers valuable mechanistic insights.
Core Tip: This analysis of The Cancer Genome Atlas data revealed that MEX3A mRNA expression is significantly higher in hepatocellular carcinoma (HCC) tissues compared to adjacent non-tumor tissues. High MEX3A expression was associated with worse overall survival in HCC patients. Knockdown of MEX3A in HCC cell lines (HepG2 and MHCC-97H) significantly inhibited cell proliferation and colony formation. MEX3A silencing induced cell cycle arrest at the G1 phase, accompanied by decreased expression of cyclin D1 and increased expression of the cell cycle inhibitor p21. MEX3A knockdown reduced the nuclear translocation of β-catenin (P < 0.05), a key component of the Wnt signaling pathway, and downregulated downstream targets such as c-Myc and cyclin D1. The development of treatments targeting genes with oncogenic alterations and related signaling pathways, based on advances in understanding of molecular cancer biology, is a major step in cancer treatment evolution.
