# Helicobacter pylori Promoted miR-196a/b-5p Expression and Accelerated Tumorigenesis of the Gastric Mucosa by Targeting IGF2BP1 and Activating PI3K-Akt Signaling Pathway

## TL;DR

This study shows how Helicobacter pylori infection increases miR-196a/b-5p levels, which promotes stomach cancer by targeting IGF2BP1 and activating the PI3K-Akt pathway.

## Contribution

The study identifies miR-196a/b-5p as a novel driver of gastric cancer progression linked to H. pylori infection and IGF2BP1 suppression.

## Key findings

- miR-196a/b-5p is upregulated in H. pylori-infected gastric tissues and cancer cells.
- miR-196a/b-5p targets IGF2BP1, reducing its tumor-suppressive effect.
- Activation of the PI3K-Akt pathway by miR-196a/b-5p promotes gastric cancer progression.

## Abstract

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).

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.

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.

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.