MicroRNA Influence in Helicobacter Pylori-Associated Gastric Carcinogenesis

Gastric cancer remains a leading cause of cancer mortality worldwide, and chronic infection with Helicobacter pylori is its most important environmental risk factor. MicroRNAs (miRNAs) have emerged as pivotal regulators in the multistep cascade from chronic gastritis through preneoplastic changes to invasive carcinoma. By fine‐tuning gene expression post-transcriptionally, miRNAs influence cell proliferation, apoptosis, invasion and the inflammatory milieu that H. pylori establishes. Key bacterial virulence factors, notably the CagA oncoprotein, activate host signalling pathways such as NF-κB, leading to dysregulated miRNA profiles. Aberrant miRNA expression can target tumour suppressor genes or promote oncogenes, amplifying neoplastic progression. Furthermore, extracellular vesicles, or exosomes, act as vehicles for miRNA transfer, extending pathogenic effects beyond the gastric mucosa and contributing to systemic complications. Understanding these networks offers prospects for novel biomarkers and therapeutic targets in H. pylori-driven gastric carcinogenesis.

Research from Nature Portfolio

A foundational study evaluated miRNA expression across stages of Correa’s cascade, demonstrating that miR-155 and miR-223 levels gradually rise from chronic non-atrophic gastritis through atrophic gastritis to carcinoma. By profiling antral and corpus mucosa, researchers established a miRNA-based score capable of discriminating preneoplastic lesions with high accuracy. The regional specificity of miRNA expression underlines the importance of sampling site in future biomarker development. This work elucidates how preneoplastic mucosa acquires a distinct miRNA signature, highlighting diagnostic and stratification potential in early gastric neoplasia.

MicroRNA Influence in Helicobacter Pylori-Associated Gastric Carcinogenesis publication trend

The graph below shows the total number of articles in microrna influence in helicobacter pylori-associated gastric carcinogenesis across all publications each year (not limited to Nature Index journals).

Technical terms

microRNA (miRNA): Small non-coding RNA molecules (~18–24 nucleotides) that bind messenger RNAs to repress translation or induce degradation, thus regulating gene expression post-transcriptionally.

Helicobacter pylori: A Gram-negative, spiral bacterium that colonises the gastric mucosa and is implicated in chronic gastritis, peptic ulcers and gastric cancer.

Exosome: Extracellular vesicles (30–150 nm) released by cells, carrying proteins, lipids and RNA, which mediate intercellular communication and can disseminate pathogenic signals.

NF-κB: A transcription factor central to inflammatory and immune responses; upon activation, it translocates to the nucleus to regulate genes involved in cell survival and cytokine production.

CagA (cytotoxin-associated gene A): A major H. pylori virulence protein injected into host cells via a type IV secretion system, modulating signalling pathways and contributing to oncogenesis.

References

1. Helicobacter pylori induced miR-362-5p upregulation drives gastric cancer progression and links hepatocellular carcinoma through an exosome-dependent pathway. Frontiers in Cellular and Infection Microbiology (2025).
2. NF-κB/miR-223-3p/ARID1A axis is involved in Helicobacter pylori CagA-induced gastric carcinogenesis and progression. Cell Death & Disease (2018).
3. Differential expression of microRNAs in preneoplastic gastric mucosa. Scientific Reports (2015).
4. MicroRNA Modulation of Host Immune Response and Inflammation Triggered by Helicobacter pylori. International Journal of Molecular Sciences (2021).