ArticleThe Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology2025
Helicobacter pylori Promoted miR-196a/b-5p Expression and Accelerated Tumorigenesis of the Gastric Mucosa by Targeting IGF2BP1 and Activating PI3K-Akt Signaling Pathway.
Article in The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Helicobacter pylori-Induced Persistent IGF2BP1 Activation Promotes Ferroptosis Resistance in Gastric Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/Aims: The study focuses on examining the impact of Helicobacter pylori (H. pylori) on the modulation of the miRNA expression profiles while also unraveling the associated pathways that play a significant role in initiating and driving the development of gastric cancer (GC). Materials and Methods: An in-depth analysis of miRNA expression profiles in gastric tissue samples from patients with chronic superficial gastritis (CSG), chronic atrophic gastritis (CAG), dysplasia (Dys), or GC was conducted. The carbon-13 urea breath test was used to identify H. pylori infection, and the participant cohort was characterized by the presence of H. pylori infection. Additionally, the role of miR-196a/b-5p in GC carcinogenesis was investigated. Results: A total of five miRNAs-miR-196a-5p, 196b-5p, 224-5p, 424-3p, and 941-demonstrated marked elevation in CSG, CAG, Dys, and GC. miR-196a/b-5p was observed to be upregulated in GC cells following H. pylori infection, as well as in Dys and GC tissue samples from patients harboring H. pylori. miR-196a/b-5p can expedite GC progression. Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1), the target gene of miR-196a/b-5p, diminishes the proliferation capability of GC cells; however, miR-196a/b-5p can partially counteract this effect. miR-196a/b-5p activates the PI3K-Akt pathway, while IGF2BP1 inhibits the expression of these proteins. Conclusion: The levels of miR-196a/b-5p were observed to escalate following H. pylori infection, subsequently fostering the progression of GC by specifically targeting IGF2BP1 and triggering the PI3K-Akt signaling cascade.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.