Li Z, Zhang B, Hu KF, Cao CL. Hsa_circ_0003848 promotes gastric cancer via miR-144-3p/mesenchymal-epithelial transition factor and serves as a plasma biomarker in Helicobacter pylori infection. World J Gastrointest Oncol 2026; 18(6): 118678 [DOI: 10.4251/wjgo.v18.i6.118678]
Corresponding Author of This Article
Chun-Li Cao, MD, The Second Affiliated Hospital of Jiaxing University, 1518 Huancheng North Road, Jiaxing 314000, Zhejiang Province, China. liswan95@foxmail.com
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Oncology
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research-article
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Li Z, Zhang B, Hu KF, Cao CL. Hsa_circ_0003848 promotes gastric cancer via miR-144-3p/mesenchymal-epithelial transition factor and serves as a plasma biomarker in Helicobacter pylori infection. World J Gastrointest Oncol 2026; 18(6): 118678 [DOI: 10.4251/wjgo.v18.i6.118678]
World J Gastrointest Oncol. Jun 15, 2026; 18(6): 118678 Published online Jun 15, 2026. doi: 10.4251/wjgo.v18.i6.118678
Hsa_circ_0003848 promotes gastric cancer via miR-144-3p/mesenchymal-epithelial transition factor and serves as a plasma biomarker in Helicobacter pylori infection
Zhe Li, Bo Zhang, Ke-Feng Hu, Chun-Li Cao
Zhe Li, Bo Zhang, Ke-Feng Hu, Department of Gastroenterology, The First Affiliated Hospital of Ningbo University, Ningbo 315010, Zhejiang Province, China
Chun-Li Cao, The Second Affiliated Hospital of Jiaxing University, Jiaxing 314000, Zhejiang Province, China
Author contributions: Li Z was responsible for collection and assembly of data; Li Z, Zhang B and Hu KF were responsible for provision of study materials or patients, prepared figures; Li Z, Zhang B and Cao CL were responsible for data analysis and interpretation, wrote the main manuscript text, performed experiments and verified the results; Li Z and Cao CL were responsible for administrative support; all authors were responsible for conception and design, reviewed the manuscript and approved the final version to be published.
Supported by Medical and Health Research Project of Zhejiang Province, No. 2023RC262 and No. 2024KY1491; and Ningbo Top Medical and Health Research Program, No. 2023020612.
Institutional review board statement: This study was approved by the Ethics Committee of the First Affiliated Hospital of Ningbo University, No. 2023176A-02.
Conflict-of-interest statement: All authors declare no conflict of interest in publishing the manuscript.
Data sharing statement: All data generated or analyzed during this study are included in this published article.
Corresponding author: Chun-Li Cao, MD, The Second Affiliated Hospital of Jiaxing University, 1518 Huancheng North Road, Jiaxing 314000, Zhejiang Province, China. liswan95@foxmail.com
Received: January 9, 2026 Revised: February 2, 2026 Accepted: March 19, 2026 Published online: June 15, 2026 Processing time: 152 Days and 7.4 Hours
Abstract
BACKGROUND
As non-coding RNA molecules, circular RNAs exhibit high stability and tissue-specific expression, and accumulating evidence indicates their critical roles in the progression and prognosis of gastric cancer (GC). However, the functional mechanisms of many circular RNAs remain unclear. This study focuses on hsa_circ_0003848, exploring its involvement in malignant GC phenotypes and its underlying molecular signaling, particularly in the context of Helicobacter pylori (H. pylori) infection. The experimental strategy combines loss-of-function and gain-of-function approaches.
AIM
To investigate the hsa_circ_0003848’s oncogenic role and biomarker potential in H. pylori-positive GC.
METHODS
Expression of hsa_circ_0003848 was detected in paired GC tissues, adjacent non-tumor tissues, and plasma from GC patients/healthy controls. Bioinformatics analysis was performed to predict target miRNAs. SiRNA-mediated hsa_circ_0003848 knockdown was achieved in GC cells, followed by cell counting kit-8, wound-healing/Transwell migration and apoptosis assays. Dual-luciferase reporter and AGO2-RIP assays were conducted to validate RNA interactions; mesenchymal-epithelial transition factor (MET)-overexpression rescue experiments were performed to confirm the functional axis.
RESULTS
Hsa_circ_0003848 was significantly upregulated in both GC tissues and plasma, with particularly elevated levels in H. pylori-positive patients, demonstrating strong diagnostic potential (e.g., high area under the curve in receiver operating characteristic analysis). Knockdown of hsa_circ_0003848 suppressed GC cell proliferation and migration while inducing apoptosis. Mechanistically, hsa_circ_0003848 functioned as a competing endogenous RNA by directly binding to and sequestering hsa-miR-144-3p, thereby relieving miR-144-3p-mediated repression of MET. Overexpression of MET effectively reversed the anti-migratory effects caused by hsa_circ_0003848 silencing, confirming the hsa_circ_0003848/miR-144-3p/MET regulatory axis.
CONCLUSION
Hsa_circ_0003848 promotes GC by sponging miR-144-3p to upregulate MET, showing promise as a non-invasive biomarker and therapeutic target, especially in H. pylori-positive cases.
Core Tip: Hsa_circ_0003848 is significantly upregulated in gastric cancer, particularly in Helicobacter pylori-positive cases, and functions as an oncogenic competing endogenous RNA by sponging miR-144-3p to activate mesenchymal-epithelial transition factor signaling. Its detectable elevation in plasma highlights its dual potential as a non-invasive diagnostic biomarker and a promising therapeutic target.
