Sun NQ, Zhang HX, Mo SJ. Letter to the Editor: Icaritin targeting epithelial-mesenchymal transition in colorectal cancer. World J Gastrointest Oncol 2026; 18(9): 119926 [DOI: 10.4251/wjgo.119926]
Corresponding Author of This Article
Sai-Jun Mo, PhD, Associate Professor, Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, No. 100 Science Avenue, Zhongyuan District, Zhengzhou 450001, Henan Province, China. sjmo@zzu.edu.cn
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Oncology
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letter
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Sun NQ, Zhang HX, Mo SJ. Letter to the Editor: Icaritin targeting epithelial-mesenchymal transition in colorectal cancer. World J Gastrointest Oncol 2026; 18(9): 119926 [DOI: 10.4251/wjgo.119926]
World J Gastrointest Oncol. Sep 15, 2026; 18(9): 119926 Published online Sep 15, 2026. doi: 10.4251/wjgo.119926
Letter to the Editor: Icaritin targeting epithelial-mesenchymal transition in colorectal cancer
Na-Qi Sun, Han-Xiao Zhang, Sai-Jun Mo
Na-Qi Sun, Han-Xiao Zhang, Sai-Jun Mo, Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, Henan Province, China
Na-Qi Sun, The Third Clinical School of Zhengzhou University, Zhengzhou 450000, Henan Province, China
Co-first authors: Na-Qi Sun and Han-Xiao Zhang.
Author contributions: Sun NQ composed the manuscript and participated in the revision of the manuscript; Zhang HX participated in the revision of the manuscript; Sun NQ and Zhang HX contributed equally to this article, they are the co-first authors of this manuscript; Mo SJ provided the research idea and participated in the revision of the manuscript; and all authors have read and approved the final manuscript.
AI contribution statement: We used the following AI tools for language polishing: DeepSeek, Grammarly, and the paid AI writing assistant service “BiMuyu”. All core content of the manuscript (including the abstract, introduction, materials and methods, results, discussion, and conclusion) was independently written by myself. No part of the main text was generated by artificial intelligence. The aforementioned AI tools were only used for language polishing, including grammar correction, sentence structure optimization, and improving the readability and fluency of the text. They were not used for data analysis or any part of the writing process itself. No AI tool was involved in the study design, data interpretation, or any other part of the research process. No image in the manuscript was generated by artificial intelligence.
Supported by the Foundation of Henan Educational Committee, No. 26A310017; and the College Student Innovation and Entrepreneurship Competitions, No. 202510459174 and No. 2025cxcy639.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Sai-Jun Mo, PhD, Associate Professor, Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, No. 100 Science Avenue, Zhongyuan District, Zhengzhou 450001, Henan Province, China. sjmo@zzu.edu.cn
Received: February 10, 2026 Revised: March 6, 2026 Accepted: April 22, 2026 Published online: September 15, 2026 Processing time: 196 Days and 22.9 Hours
Abstract
This commentary critically evaluates the study by Li et al published in the World Journal of Gastrointestinal Oncology, which suggests that icaritin may inhibit colorectal cancer (CRC) metastasis by reversing epithelial-mesenchymal transition and suppressing Wnt/β-catenin signaling in preclinical models. While the findings are promising, the evidence remains insufficient, as alterations in protein expression alone do not confirm modulation of the pathway. Further research is necessary to demonstrate that icaritin effectively inhibits migration and invasion through Wnt/β-catenin signaling in CRC. In addition to assessing changes in the protein levels of core pathway components, examining target localization and conducting rescue experiments with pathway activators or inhibitors would provide robust evidence of pathway dependence. To facilitate clinical application, a systematic pathway from target validation to formulation optimization and clinical testing is necessary. Enhanced formulations that tackle poor solubility and low bioavailability, coupled with comprehensive clinical trials to confirm efficacy and safety, are critical. Addressing these deficiencies will create a solid foundation for icaritin as a promising therapeutic strategy in the management of CRC.
Core Tip: This commentary evaluates the study by Li et al, which suggests that icaritin inhibits colorectal cancer metastasis by reversing epithelial-mesenchymal transition and suppressing Wnt/β-catenin signaling. Although the findings are promising, changes in protein expression alone do not adequately confirm modulation of the pathway. Further research is necessary, including target localization studies and rescue experiments utilizing pathway activators, inhibitors, or gene modulation, to establish the dependence on Wnt/β-catenin signaling. For clinical translation, it is essential to validate targets, develop improved formulations to address issues of poor solubility and bioavailability, and conduct clinical trials to verify both efficacy and safety. Addressing these gaps will be crucial in establishing icaritin as a viable therapeutic strategy for the management of colorectal cancer.
