Basic Study
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World J Gastrointest Oncol. Mar 15, 2024; 16(3): 979-990
Published online Mar 15, 2024. doi: 10.4251/wjgo.v16.i3.979
Effects of Helicobacter pylori and Moluodan on the Wnt/β-catenin signaling pathway in mice with precancerous gastric cancer lesions
Yi-Mei Wang, Zheng-Wei Luo, Yu-Lin Shu, Xiu Zhou, Lin-Qing Wang, Chun-Hong Liang, Chao-Qun Wu, Chang-Ping Li
Yi-Mei Wang, Zheng-Wei Luo, Yu-Lin Shu, Xiu Zhou, Lin-Qing Wang, Chun-Hong Liang, Chao-Qun Wu, Chang-Ping Li, Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan Province, China
Author contributions: Wang YM was responsible for purchasing materials, conducting relevant experiments, and writing articles; Luo ZW was responsible for designing the experimental plan and assisting in completing the experiment and the article; Shu YL, Zhou X, and Wang LQ were responsible for assisting in completing experiments; Liang CH and Wu CQ was responsible for helping to collect data; Li CP was responsible for guiding experiments and methods and editing the article; all authors approved the final version of the article.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Southwest Medical University (Protocol No. SWMU20230818).
Conflict-of-interest statement: There is no conflicting interest about this article.
Data sharing statement: No additional data are available.
ARRIVE guidelines statement: The authors have read the ARRIVE Guidelines, and the manuscript was prepared and revised according to the ARRIVE Guidelines.
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: Chang-Ping Li, MM, Academic Editor, Additional Professor, Doctor, Professor, Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, No. 25 Taiping Street, Luzhou 646000, Sichuan Province, China. 506854209@qq.com
Received: October 11, 2023
Peer-review started: October 11, 2023
First decision: December 8, 2023
Revised: December 16, 2023
Accepted: January 24, 2024
Article in press: January 24, 2024
Published online: March 15, 2024
Processing time: 152 Days and 17.8 Hours
Abstract
BACKGROUND

Helicobacter pylori (H. pylori) is the primary risk factor for gastric cancer (GC), the Wnt/β-Catenin signaling pathway is closely linked to tumourigenesis. GC has a high mortality rate and treatment cost, and there are no drugs to prevent the progression of gastric precancerous lesions to GC. Therefore, it is necessary to find a novel drug that is inexpensive and preventive to against GC.

AIM

To explore the effects of H. pylori and Moluodan on the Wnt/β-Catenin signaling pathway and precancerous lesions of GC (PLGC).

METHODS

Mice were divided into the control, N-methyl-N-nitrosourea (MNU), H. pylori + MNU, and Moluodan groups. We first created an H. pylori infection model in the H. pylori + MNU and Moluodan groups. A PLGC model was created in the remaining three groups except for the control group. Moluodan was fed to mice in the Moloudan group ad libitum. The general condition of mice were observed during the whole experiment period. Gastric tissues of mice were grossly and microscopically examined. Through quantitative real-time PCR (qRT-PCR) and Western blotting analysis, the expression of relevant genes were detected.

RESULTS

Mice in the H. pylori + MNU group showed the worst performance in general condition, gastric tissue visual and microscopic observation, followed by the MNU group, Moluodan group and the control group. QRT-PCR and Western blotting analysis were used to detect the expression of relevant genes, the results showed that the H. pylori + MNU group had the highest expression, followed by the MNU group, Moluodan group and the control group.

CONCLUSION

H. pylori can activate the Wnt/β-catenin signaling pathway, thereby facilitating the development and progression of PLGC. Moluodan suppressed the activation of the Wnt/β-catenin signaling pathway, thereby decreasing the progression of PLGC.

Keywords: Helicobacter pylori; Gastric cancer; Wnt/β-catenin signaling pathway; Moluodan

Core Tip: Helicobacter pylori (H. pylori) is a pathological bacteria. We explored the effects of H. pylori and the traditional Chinese medicine Moluodan on the Wnt/β-Catenin signaling pathway and precancerous lesions of GC (PLGC). Our experiments successfully established a mouse model of H. pylori infection and PLGC, which serves as a reference for others. Through the gene expression assay, we concluded that H. pylori accelerates the progression of PLGC by promoting the expression of Wnt/β-Catenin signaling pathway, epidermal growth factor (EGF) and c-Myc. Meanwhile, Moluodan can repair the gastric mucosa and delay the progression of PLGC by inhibiting the Wnt/β-Catenin signaling pathway and the expression of EGF and c-Myc.