Zhou X, Wang LQ, Song S, Xu M, Li CP. Helicobacter pylori infection promotes the progression of gastric cancer by regulating the expression of DMBT1. World J Clin Oncol 2025; 16(5): 105322 [DOI: 10.5306/wjco.v16.i5.105322]
Corresponding Author of This Article
Chang-Ping Li, MD, Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, No. 25 Taiping Street, Luzhou 646000, Sichuan Province, China. 506854209@qq.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
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/
World J Clin Oncol. May 24, 2025; 16(5): 105322 Published online May 24, 2025. doi: 10.5306/wjco.v16.i5.105322
Helicobacter pylori infection promotes the progression of gastric cancer by regulating the expression of DMBT1
Xiu Zhou, Lin-Qing Wang, Shuai Song, Mei Xu, Chang-Ping Li
Xiu Zhou, Lin-Qing Wang, Shuai Song, Mei Xu, Chang-Ping Li, Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan Province, China
Co-first authors: Xiu Zhou and Lin-Qing Wang.
Author contributions: Zhou X and Wang LQ contributed equally as co-first authors; Zhou X designed the experimental plan, conducted relevant experiments, and wrote the original article; Wang LQ conducted relevant experiments, collected data and performed statistical analysis of data; Song S acquired materials, assisted in conducting experiments, and supplemented the article; Xu M assisted in completing experiments; Li CP supervised experiments and methods, and edited the article. All authors read and approved the final manuscript.
Institutional review board statement: The study was reviewed and approved by the Institutional Clinical Trial Ethics Committee of Affiliated Hospital of the Southwest Medical University (Approval No.KY2025054).
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Data sharing statement: No additional data are available.
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, MD, Department of Gastroenterology, The Affiliated Hospital of Southwest Medical University, No. 25 Taiping Street, Luzhou 646000, Sichuan Province, China. 506854209@qq.com
Received: January 18, 2025 Revised: March 4, 2025 Accepted: March 26, 2025 Published online: May 24, 2025 Processing time: 122 Days and 12.5 Hours
Abstract
BACKGROUND
Each year, more than a million people are diagnosed with gastric cancer (GC) worldwide, and the incidence of this disease is projected to increase. Helicobacter pylori (H. pylori) is the major cause of GC. Managing infections caused by H. pylori and investigating their contribution to GC carcinogenesis are crucial for advancing diagnosis and treatment. Deleted in malignant brain tumors 1 (DMBT1) is associated with the development of H. pylori and GC. However, the precise underlying mechanism is unclear.
AIM
To explore the role of DMBT1, as modulated by H. pylori, in the development, proliferation, and metastasis of GC.
METHODS
Utilizing human GC cells, DMBT1 gene silencing, and H. pylori treatment, four cell groups (control, H. pylori, si-DMBT1, and H. pylori + si-DMBT1) were subjected to cell counting kit-8, scratch, and Transwell assays. The DMBT1 expression was assessed by quantitative real-time polymerase chain reaction and Western blot.
RESULTS
In cellular tests, H. pylori + si-DMBT1 showed the greatest ability to proliferate, migration, and invasion capabilities, followed by the si-DMBT1, H. pylori, and control groups. DMBT1 mRNA was found to be the highest in control group, next in si-DMBT1, H. pylori and H. pylori + si-DMBT1, while H. pylori + si-DMBT1 showed the least expression. The results the Western blot assay showed a consistent trend of decreasing DMBT1 protein and mRNA levels.
CONCLUSION
Through inhibition of DMBT1, H. pylori could enhance GC’s proliferation, metastasis and invasion. Our findings revealed a novel connection between H. pylori infection, inflammation, and GC.
Core Tip: The main reason for gastric cancer (GC) is Helicobacter pylori (H. pylori). The annual global burden of GC continues to increase. Our study investigated the influence of deleted in malignant brain tumors 1 induced by H. pylori on the proliferation and metastasis of GC. Using human GC cells, we concluded that H. pylori promote GC cell proliferation, metastasis, and invasion through down-regulation of deleted in malignant brain tumors 1 and facilitates GC development through cell function experiments and gene expression experiments.
