Taurine suppresses gastric intestinal metaplasia in patient-derived organoids and Atp4a-/- mice

doi:10.4251/wjgo.v18.i2.114161

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Feb 15, 2026 (publication date) through Feb 3, 2026

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World Journal of Gastrointestinal Oncology

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1948-5204

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastrointest Oncol. Feb 15, 2026; 18(2): 114161
Published online Feb 15, 2026. doi: 10.4251/wjgo.v18.i2.114161

Taurine suppresses gastric intestinal metaplasia in patient-derived organoids and Atp4a^-/- mice

Ke Liu, Xi Zhang, Fa-Zhan Li, Peng-Yuan Zheng, Yang Mi

Ke Liu, Xi Zhang, Fa-Zhan Li, Peng-Yuan Zheng, Yang Mi, Henan Key Laboratory for Helicobacter pylori and Digestive Tract Microecology, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, China

Peng-Yuan Zheng, Yang Mi, Institute of Rehabilitation Medicine, Henan Academy of Innovations in Medical Science, Zhengzhou 450003, Henan Province, China

Peng-Yuan Zheng, Yang Mi, Tianjian Laboratory of Advanced Biomedical Sciences, Zhengzhou University, Zhengzhou 450000, Henan Province, China

Co-first authors: Ke Liu and Xi Zhang.

Author contributions: Liu K and Zhang X contributed equally to this study as co-first authors; Liu K and Mi Y conceived and designed the experiments and performed most of the experiments; Liu K, Li FZ, and Zhang X analyzed the data; Liu K, Zheng PY, and Zhang X interpreted all of the results and wrote the manuscript; All of the authors have read and approved the final manuscript and agreed to be accountable for all aspects of the work.

Supported by Tianjian Advanced Biomedical Laboratory Key Research and Development Project; Henan Province Natural Science Foundation, No. 242300421283.

Institutional review board statement: The human study protocol was reviewed and approved by the Medical Ethics Committee of the Fifth Affiliated Hospital of Zhengzhou University (Approval No. KY2025038-K02).

Institutional animal care and use committee statement: All animal experiments were approved by the Animal Ethics Committee of the Fifth Affiliated Hospital of Zhengzhou University (Approval No. KY-Y-2025059) and were performed in compliance with institutional and national guidelines for the care and use of laboratory animals.

Conflict-of-interest statement: The authors have no conflicts of interest to declare.

ARRIVE guidelines statement: The authors have read the ARRIVE guidelines, and the manuscript was prepared and revised according to the ARRIVE guidelines.

Data sharing statement: De-identified data generated or analyzed in this study are available from the corresponding author upon reasonable request. Human tissue samples and organoid materials cannot be shared due to privacy protection and ethical restrictions specified in the informed consent form.

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: Yang Mi, PhD, Henan Key Laboratory for Helicobacter pylori and Digestive Tract Microecology, The Fifth Affiliated Hospital of Zhengzhou University, No. 3 Kangfu Qianjie, Erqi District, Zhengzhou 450052, Henan Province, China. yangmi198@zzu.edu.cn

Received: September 15, 2025
Revised: November 23, 2025
Accepted: December 16, 2025
Published online: February 15, 2026
Processing time: 143 Days and 17.5 Hours

Abstract

BACKGROUND

Gastric intestinal metaplasia (GIM) represents a critical precancerous condition in the progression from chronic gastritis to gastric cancer, with limited therapeutic options. Emerging evidence suggests that taurine, a cytoprotective amino acid, may modulate gastric epithelial dysfunction. However, its application and efficiency in the context of GIM remain poorly understood.

AIM

To investigate the therapeutic effects of taurine on GIM using patient-derived organoids and Atp4a^-/- mouse models.

METHODS

Patient-derived GIM organoids (n = 3) and Atp4a^-/- mice, which spontaneously develop GIM, were used as experimental models. Morphological changes were assessed via Alcian blue-periodic acid Schiff staining. The expression levels of the gastric epithelial marker mucin 5AC (MUC5AC) and GIM-associated markers (caudal type homeobox 2 [CDX2], MUC2, Trefoil factor family 3 [TFF3]) were quantified via quantitative PCR, Western blotting, and immunohistochemistry.

RESULTS

We confirmed that taurine treatment significantly attenuated pathological changes, including glandular hypertrophy and vacuolar dilation, in Atp4a^-/- mice. It also reduced GIM severity compared with that in the untreated model group. Under taurine treatment, MUC5AC expression was significantly increased, whereas the intestinal-specific markers CDX2, MUC2, and TFF3 were reduced (P < 0.05). In parallel, in patient-derived GIM organoids, taurine treatment significantly ameliorated GIM features, as evidenced by increased MUC5AC expression and decreased CDX2, MUC2, and TFF3 expression.

CONCLUSION

This study highlights the potential application of taurine as a therapeutic agent for treating GIM, offering a promising strategy for its clinical management.

Keywords: Atp4a gastric intestinal metaplasia models; Biomarkers; Gastric intestinal metaplasia; Organoid; Taurine

Core Tip: Limited treatments for gastric intestinal metaplasia (GIM) are available. This study used Atp4a^-/- mice (spontaneous GIM models) and patient-derived GIM organoids to show that taurine ameliorates GIM. It reduces murine gastric mucosal lesions, upregulates the gastric marker mucin 5AC (MUC5AC), and downregulates intestinal markers (caudal type homeobox 2, MUC2, and Trefoil factor family 3) in both models, suggesting a novel GIM therapeutic strategy.