This review highlights the role of therapeutic targets and inflammation in gastric cancer associated with Helicobacter pylori.
Gastric cancer (GC) remains a complex disorder with an unclear etiology. Helicobacter pylori , a Gram‐negative bacterium, plays a key role in the development of chronic gastritis, peptic ulcers, anemia, and GC. It survives and proliferates in macrophage autophagosomes, gastric epithelial cells, and dendritic cells, with its cytotoxin‐associated gene A ( CagA ) and vacuolating Toxin A ( VacA ) interfering with autophagy. While most infected patients develop chronic gastritis, 10%–15% develop ulcers, and 1%–3% progress to GC. MicroRNAs (miRNAs), small noncoding RNAs, regulate genes by modulating tumor suppressors and oncogenes, and are crucial in GC. This review explores miRNAs as potential biomarkers and therapeutic targets for early GC diagnosis, monitoring progression, and predicting treatment outcomes. Dysregulated miRNAs such as miR‐124, miR‐145, and miR‐21 have been identified in GC. Additionally, miRNAs influence H. pylori ‐induced inflammation and the expression of virulence factors. Targeting miRNAs could reduce H. pylori ‐related diseases, including gastritis, ulcers, and GC. However, further research is required to fully understand miRNAs’ role in H. pylori infection and develop miRNA‐based therapies.
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Sariani et al. (2025) studied this question.
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