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Infection with  Helicobacter pylori  ( H. pylori ) and the resulting gastric inflammation is regarded as the strongest risk factor for gastric carcinogenesis and progression. NF-κB plays an important role in linking  H. pylori- mediated inflammation to cancer. However, the underlying mechanisms are poorly understood. In this study, we find that  H. pylori  infection induces miR-223-3p expression in   H. pylori  CagA-dependent manner. NF-κB stimulates miR-223-3p expression via directly binding to the promoter of miR-223-3p and is required for  H. pylori  CagA-mediated upregulation of miR-223-3p. miR-223-3p promotes the proliferation and migration of gastric cancer cells by directly targeting ARID1A and decreasing its expression. Furthermore, miR-223-3p/ARID1A axis is involved in CagA-induced cell proliferation and migration. In the clinical setting, the level of miR-223-3p is upregulated, while ARID1A is downregulated significantly in human gastric cancer tissues compared with the corresponding noncancerous tissues. The expression level of miR-223-3p is significantly higher in  H. pylori -positive gastric cancer tissues than that in  H. pylori- negative tissues. Moreover, a negative correlation between miR-223-3p and ARID1A expression is found in the gastric cancer tissues. Taken together, our findings suggested NF-κB/miR-223-3p/ARID1A axis may link the process of  H. pylori -induced chronic inflammation to gastric cancer, thereby providing a new insight into the mechanism underlying  H. pylori -associated gastric diseases.

NF-κB/miR-223-3p/ARID1A axis is involved in Helicobacter pylori CagA-induced gastric carcinogenesis and progression