Hua YQ, Guo KX, Ni P, Wang D, An TY, Gao YY, Zhang RG. RPF2 regulates the protein kinase B/mammalian target of rapamycin pathway in the pathogenesis of Helicobacter pylori. World J Gastrointest Oncol 2025; 17(6): 105664 [DOI: 10.4251/wjgo.v17.i6.105664]
Corresponding Author of This Article
Rong-Guang Zhang, MD, Professor, Department of Epidemiology, College of Public Health, Zhengzhou University, No. 100 Science Avenue, Zhongyuan District, Zhengzhou 450001, Henan Province, China. zrg@zzu.edu.cn
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 Gastrointest Oncol. Jun 15, 2025; 17(6): 105664 Published online Jun 15, 2025. doi: 10.4251/wjgo.v17.i6.105664
RPF2 regulates the protein kinase B/mammalian target of rapamycin pathway in the pathogenesis of Helicobacter pylori
Yan-Qiao Hua, Kai-Xin Guo, Peng Ni, Di Wang, Tong-Yan An, Yang-Ye Gao, Rong-Guang Zhang
Yan-Qiao Hua, Kai-Xin Guo, Peng Ni, Di Wang, Tong-Yan An, Yang-Ye Gao, Rong-Guang Zhang, Department of Epidemiology, College of Public Health, Zhengzhou University, Zhengzhou 450001, Henan Province, China
Kai-Xin Guo, Department of Occupational Disease Control, Anyang Center for Disease Control and Prevention, Anyang 455000, Henan Province, China
Rong-Guang Zhang, Heinz Mehhorn Academician Workstation, School of Public Health, Hainan Medical University, Haikou 571199, Hainan Province, China
Author contributions: Hua YQ, Ni P and Zhang RG designed the research study; Hua YQ, Guo KX, Wang D, An TY and Gao YY performed experiments; Hua YQ and Guo KX analyzed the data; Hua YQ and Zhang RG wrote the manuscript; All authors have read and approved the final manuscript.
Supported by the National Natural Science Foundation of China, No. 82160634.
Institutional review board statement: The study was conducted in vitro and did not involve human subjects.
Institutional animal care and use committee statement: The study was conducted in vitro and did not involve any animal subjects.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Data sharing statement: The experimental data that support the findings of this study are available from the corresponding author at zrg@zzu.edu.cn.
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: Rong-Guang Zhang, MD, Professor, Department of Epidemiology, College of Public Health, Zhengzhou University, No. 100 Science Avenue, Zhongyuan District, Zhengzhou 450001, Henan Province, China. zrg@zzu.edu.cn
Received: February 10, 2025 Revised: March 25, 2025 Accepted: May 12, 2025 Published online: June 15, 2025 Processing time: 124 Days and 17.3 Hours
Abstract
BACKGROUND
RPF2 is a crucial factor in ribosome synthesis, which has been linked to the development of several cancers. However, the mechanism of RPF2 in gastric carcinogenesis is unclear.
AIM
To explore the role and mechanism of RPF2 in the pathogenesis of Helicobacter pylori (H. pylori) infection.
METHODS
GES-1 was co-cultured with H. pylori in vitro to detect changes in the expression of RPF2. Overexpression and silencing of RPF2 were performed. Quantitative real-time polymerase chain reaction (q-PCR) and Western blot (WB) were used to determine mRNA and protein expression of RPF2, protein kinase B (AKT)/mammalian target of rapamycin (mTOR), and epithelial-mesenchymal transition-related factors MMP2 and MMP9; cell counting kit 8 and wound healing assays were utilized to evaluate cell viability and migratory capacity; q-PCR, WB, and immunohistochemistry were employed to establish RPF2 expression in cancer tissues.
RESULTS
H. pylori facilitated RPF2 expression and triggered AKT/mTOR signaling pathway. Functional experiments showed that RPF2 overexpression could promote a series of malignant transformations such as cell proliferation, cell migration and invasion, and further enhance AKT/mTOR signaling pathway activation. RPF2 knockdown had the opposite effect. In addition, RPF2 expression was higher in gastric cancer tissues than in adjacent tissues.
CONCLUSION
RPF2 plays a significant role in the pathogenic mechanism of H. pylori infection and may be useful in the detection and management of gastric cancer caused by H. pylori infection.
Core Tip: Helicobacter pylori (H. pylori) has a profound impact on gastric cancer development. RPF2 is overexpressed in cancer and can enhance cancer cell proliferation. However, the mechanism of RPF2 in the pathogenesis of H. pylori infection remains largely unknown. We found that H. pylori infection increased RPF2 expression, affecting the malignant behavior of gastric epithelial cells by regulating the protein kinase B/mammalian target of rapamycin pathway. This study is the first to explore the mechanism of RPF2 in the pathogenesis of H. pylori infection.
