Study on the Probiotics Regulating miRNA in H. Pylori-induced Wnt/β-catenin Gastric Carcinogenesis.

NCT05544396 | Active Not Recruiting

• 1 other identifier: A-BR-106-085
• Study Type: interventional
• Target: 100
• Locations: 1 country
• Sites: 1

Brief Summary

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. 1.to establish the H. pylori induces the Wnt/beta-catenin and COX-2 signaling pathway in vitro.
2. 2.to investigate the effects and mechanisms of L. acidophilus and B. latis on H. pylori-induced Wnt/beta-catenin oncogenesis pathway.
3. 3.to study whether probiotics ingestion promote IM regression or ameliorate IM progression in H. pylori-infected patients after successful eradication therapy.

Conditions

H. Pylori Infection; Carcinogenesis

Keywords

H. Pylori; Wnt/beta-catenin; miRNA; carcinogenesis

Outcome Measures

Primary Outcomes (1)

• The IM regression rate one year after H. pylori eradication

  H. pylori-infected participants (n=100) with IM received successful H. pylori eradication. Group I (n=50) given oral probiotics 1 pack bid for 6 months, Group II did not treat. The 2nd panendoscopy followed at one year later to evaluate IM status using Updated Sydney System Score.

  Eligible participants allocated to treat or non-treat groups. The panendoscopy was performed one year later.

Study Arms (2)

probiotic group

EXPERIMENTAL

Routine eradicate treatment H. pylori, and probiotics (2 packs per day) for 6 months.

Other: probiotic

control group

PLACEBO COMPARATOR

Only routine eradicate treatment H. pylori.

Other: probiotic

Interventions

probiotic OTHER

probiotic group give probiotics (2 packs per day) for 6 months.

control group; probiotic group

Eligibility Criteria

• Age: 20 Years+
• Sex: all
• Healthy Volunteers: No
• Age Groups: Adult (18-64), Older Adult (65+)

You may qualify if:

• years of age or older
• Have undergone gastroscopy
• First discovered H.pylori infection and intestinal metaplasia

You may not qualify if:

• 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.

Sponsors & Collaborators

• National Cheng-Kung University Hospital: lead

Study Sites (1)

National Cheng Kung University & Hospital

Tainan, 704, Taiwan

Location

Related Publications (3)

• Sheu 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 BACKGROUND

• Hung 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 BACKGROUND

• Yang 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 DERIVED

MeSH Terms

Conditions

Carcinogenesis

Interventions

Probiotics

Condition Hierarchy (Ancestors)

Neoplastic Processes; Neoplasms; Pathologic Processes; Pathological Conditions, Signs and Symptoms

Intervention Hierarchy (Ancestors)

Dietary Supplements; Food; Diet, Food, and Nutrition; Physiological Phenomena; Food and Beverages

Study Design

• Study Type: interventional
• Phase: not applicable
• Allocation: RANDOMIZED
• Masking: NONE
• Purpose: TREATMENT
• Intervention Model: PARALLEL
• Sponsor Type: OTHER
• Responsible Party: PRINCIPAL INVESTIGATOR
• PI Title: professor

Study Record Dates

• First Submitted: July 6, 2022
• First Posted: September 16, 2022
• Study Start: March 20, 2024
• Primary Completion (Estimated): July 31, 2026
• Study Completion (Estimated): July 31, 2030
• Last Updated: November 14, 2024

Record last verified: 2024-11

Data Sharing

• IPD Sharing: Will not share

Locations

TW (1)