RESUMEN
Helicobacter pylori (H. pylori) infection plays a pivotal role in the development of gastric cancer (GC). However, the association between aberrant microRNAs (miRNAs/miRs) expression and H. pyloriinduced GC remains poorly understood. The present study reported that repeated infection of H. pylori caused the oncogenicity of GES1 cells in BALB/c Nude mice. miRNA sequencing revealed that both miR7 and miR153 were significantly decreased in the cytotoxinassociated gene A (CagA) positive GC tissues and this was further confirmed in a chronic infection model of GES1/HP cells. Further biological function experiments and in vivo experiments validated that miR7 and miR153 can promote apoptosis and autophagy, inhibit proliferation and inflammatory response in GES1/HP cells. All the associations between miR7/miR153 and their potential targets were revealed via bioinformatics prediction and dualluciferase reporter assay. Particularly, downregulation of both miR7 and miR153 obtained an improved sensitivity and specificity in diagnosing H. pylori (CagA+)induced GC. The present study identified that the combination of miR7 and miR153 may be regarded as novel therapeutic targets in H. pylori CagA (+)associated GC.