Helicobacter pylori-induced miR-136 is a potential predictor of early-stage gastric cancer

doi:10.4251/wjgo.v17.i10.109744

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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. Oct 15, 2025; 17(10): 109744
Published online Oct 15, 2025. doi: 10.4251/wjgo.v17.i10.109744

Helicobacter pylori-induced miR-136 is a potential predictor of early-stage gastric cancer

Tao Chen, An-Qiang Feng, Xiao-Ran Shen, Ni-Yi Dang, Feng Ye, Guo-Xin Zhang

Tao Chen, The First Clinical Medical College of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China

Tao Chen, An-Qiang Feng, Department of Gastroenterology, Xuzhou Central Hospital, Xuzhou 221009, Jiangsu Province, China

Xiao-Ran Shen, Department of Gastroenterology, Nantong First People’s Hospital, Nantong 226001, Jiangsu Province, China

Ni-Yi Dang, Feng Ye, Guo-Xin Zhang, Department of Gastroenterology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, Jiangsu Province, China

Co-first authors: Tao Chen and An-Qiang Feng.

Author contributions: Chen T, Feng AQ, Shen XR, Ye F, Dang NY, and Zhang GX contributed to this work; Chen T and Zhang GX contributed to the study design; Chen T, Feng AQ, and Shen XR contributed to the collection, analysis, and interpretation of data; Chen T contributed to drafting the manuscript; Zhang GX contributed to study supervision; All authors contributed to revision of the manuscript and read and approved the manuscript.

Supported by the National Natural Science Foundation of China, No. 82470593; and General Project of the Development Fund of the Affiliated Hospital of Xuzhou Medical University, No. XYFM202334.

Institutional review board statement: This study was approved by the Ethics Committee of the Xuzhou Central Hospital (Approval No. XZXY-LJ-20180627-004). All the recruited subjects signed the consent forms.

Institutional animal care and use committee statement: All animal studies (including the mice euthanasia procedure) were done in compliance with the regulations and guidelines of Xuzhou Central Hospital institutional animal care and conducted according to the AAALAC and the IACUC guidelines (Ministry of Science and Technology of China, 2006). The animal study was reviewed and approved by Xuzhou Central Hospital Animal Ethic Committee (Approval No. XZYKDX-20200721-005).

Conflict-of-interest statement: All authors report no relevant conflicts of interest for this article.

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: All data generated or analyzed during this study are included in this published article.

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: Guo-Xin Zhang, PhD, Department of Gastroenterology, The First Affiliated Hospital of Nanjing Medical University, No. 300 Guangzhou Road, Nanjing 210029, Jiangsu Province, China. nanjingmedical@163.com

Received: May 21, 2025
Revised: July 7, 2025
Accepted: August 25, 2025
Published online: October 15, 2025
Processing time: 147 Days and 4.8 Hours

Abstract

BACKGROUND

MicroRNAs play an important role in gastric cancer (GC) development following Helicobacter pylori (H. pylori) infection. Yet the exact mechanism is still not fully understood. Herein, we investigated the underlying mechanisms of miR-136 during this process.

AIM

To investigate the role of miR-136 in H. pylori-induced GC progression.

METHODS

GC and gastric epithelial cells were infected with H. pylori and transfected with miR-136 mimic, inhibitor, mimic plus PDCD11 (identified as miR-136 target), or miR-NC (control). Cell proliferation, migration, and invasion were assessed via cell counting kit-8 assay, colony formation, wound healing, and Transwell assays. Nuclear factor kappa-B (NF-κB)/miR-136/PDCD11 interactions were confirmed by luciferase and inhibition assays. For in vivo studies H. pylori-infected BGC-823 cells were injected into nude mice. Reverse transcription PCR, western blot, immunohistochemistry, and immunofluorescent staining assay were used to assess mRNA and protein expression.

RESULTS

miR-136 expression was significantly upregulated while PDCD11 expression was significantly downregulated in early GC tissues and GC cells infected with H. pylori compared with non-infected tissues or cells (all P < 0.01). miR-136 overexpression induced by H. pylori could promote the proliferation and migration of infected GC cells and induce the growth of H. pylori-positive GC tumors in mice while its inhibition could reverse this effect. Mechanistically, upregulation of miR-136 suppressed PDCD11 through NF-κB activation induced by H. pylori infection.

CONCLUSION

miR-136 is a novel diagnostic biomarker and therapeutic target in H. pylori-associated early-stage gastric carcinogenesis and acts through the NF-κB-miR-136-PDCD11 pathway.

Keywords: Helicobacter pylori; Gastric cancer; miR-136; Nuclear factor kappa-B; PDCD11

Core Tip: Helicobacter pylori infection upregulates miR-136, promoting gastric cancer progression by suppressing PDCD11 via nuclear factor kappa-B activation. This study identified miR-136 as a potential diagnostic biomarker and therapeutic target for early-stage gastric cancer, demonstrating its role in tumor growth and metastasis through in vitro and in vivo models. Targeting the nuclear factor kappa-B/miR-136/PDCD11 axis may offer new strategies for intervention.