Clinical trial · Interventional
Study on the Probiotics Regulating miRNA in H. Pylori-induced Wnt/β-catenin Gastric Carcinogenesis.
- Source
- ClinicalTrials.gov
- Retrieved
- Sep 8, 2026
- Layer
- normalized (units and labels harmonized; values unchanged)
- Run
- ING-CLINICALTRIALS-20260908-000001
Summary
Brief summary (as posted)
Background. H. pylori has recognized as a type 1 carcinogen for gastric adenocarcinoma. Although H. pylori eradication promises to reduce the risk of gastric cancer, the regression rate of intestinal metaplasia (IM) after eradication is unsatisfactory. Therefore, to find the mechanism of IM persistent and a new strategy to improve IM regression are critical for reducing gastric cancer development. The canonical Wnt/beta-catenin signaling pathway upregulating cyclooxygenase-2 (COX-2) transcriptional activity involves gastric carcinogenesis after H. pylori infection. Investigators have established an in vitro model that H. pylori induces a cagA-dependent nuclear COX-2 expression in both GES-1 and AGS cells. MicroRNAs (miRNAs) are a class of widespread non-coding RNAs and have been shown to involve in the gastric carcinogenesis. Among these gastric cancer-related miRNA candidates, some were reported to interact with Wnt/β-catenin pathway. Clinically, H. pylori eradication plus celecoxib therapy results in about one-third cases being IM regression, which correlated to the nuclear β-catenin and COX-2 expression before treatment. Based on the probiotics ingestion can ameliorate H. pylori-induced inflammatory pathways, investigators hypothesis that H. pylori eradication with probiotics supplement may promote IM regression through regulating certain miRNAs and Wnt/β-catenin signaling. The aims of this 3-year grant will 1. to establish the H. pylori induces the Wnt/beta-catenin and COX-2 signaling pathway in vitro. 2. to investigate the effects and mechanisms of L. acidophilus and B. latis on H. pylori-induced Wnt/beta-catenin oncogenesis pathway. 3. to study whether probiotics ingestion promote IM regression or ameliorate IM progression in H. pylori-infected patients after successful eradication therapy. Materials and Methods. A H. pylori (HP238) isolate strain, GES-1, and AGS cells will be used for in vitro study. The protein levels of cell tests will measured by western blot. The differences of miRNAs expression between monk, cells infected with H. pylori, and cells pretreated with probiotics than infected by H. pylori will be analyzed by next generation sequencing method. H. pylori-infected patients with IM will be randomly allocated to receive probiotics or controls, the 2nd endoscopy will be arranged at the 12th month to evaluate the IM status. Anticipated results. This study will to establish the H. pylori-induced Wnt/beta-catenin oncogenesis pathway in vitro. Furthermore, the effect and mechanism of probiotics inhibit the H. pylori-induced Wnt/beta-catenin signaling will be clarified. Finally, investigators will provide an evidence for the probiotics ingestion promote the rate of IM regression in patients after H. pylori eradication.
Conditions
Conditions (2)
Free-text conditions as registered, with the CancerIndex entity they were reconciled to and the match type.
| Condition (as posted) | Mapped entity | Match | Confidence |
|---|---|---|---|
| Carcinogenesis | — | UNRESOLVED | — |
| H. Pylori Infection | — | UNRESOLVED | — |
Interventions
Interventions (1)
| Intervention | Type | Mapped drug | Match |
|---|---|---|---|
| probiotic | Other | — | UNRESOLVED |
Design
Arms and outcomes
Arms (2)
- type
- EXPERIMENTAL
- label
- probiotic group
- description
- Routine eradicate treatment H. pylori, and probiotics (2 packs per day) for 6 months.
- interventionNames
- Other: probiotic
- type
- PLACEBO_COMPARATOR
- label
- control group
- description
- Only routine eradicate treatment H. pylori.
- interventionNames
- Other: probiotic
Primary outcomes (1)
- measure
- The IM regression rate one year after H. pylori eradication
- timeFrame
- Eligible participants allocated to treat or non-treat groups. The panendoscopy was performed one year later.
Eligibility
Eligibility (as posted)
- Sex
- All
- Minimum age
- 20 Years
Show eligibility criteria text
Inclusion Criteria: * 20 years of age or older * Have undergone gastroscopy * First discovered H.pylori infection and intestinal metaplasia Exclusion Criteria: * Massive bleeding is life-threatening * Gastric cancer * Previous treatment for H.pylori * Long-term use of non-steroidal anti-inflammatory drugs (eg, aspirin), and hydrogen ion pump inhibitors.
References
Publications (3)
- BACKGROUNDSheu BS, Tsai YC, Wu CT, Chang WL, Cheng HC, Yang HB. Long-term celecoxib can prevent the progression of persistent gastric intestinal metaplasia After H. pylori eradication. Helicobacter. 2013 Apr;18(2):117-23. doi: 10.1111/hel.12013. Epub 2012 Sep 26. PMID 23067366
- BACKGROUNDHung KH, Wu JJ, Yang HB, Su LJ, Sheu BS. Host Wnt/beta-catenin pathway triggered by Helicobacter pylori correlates with regression of gastric intestinal metaplasia after H. pylori eradication. J Med Microbiol. 2009 May;58(Pt 5):567-576. doi: 10.1099/jmm.0.007310-0. PMID 19369517
- DERIVEDYang YJ, Wu CT, Cheng HC, Chen WY, Tseng JT, Chang WL, Sheu BS. Probiotics ameliorate H. pylori-associated gastric beta-catenin and COX-2 carcinogenesis signaling by regulating miR-185. J Biomed Sci. 2025 Jun 3;32(1):55. doi: 10.1186/s12929-025-01149-3. PMID 40462044