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Gastric cancer is an important cause of death worldwide with  Helicobacter pylori  ( H. pylori ) considered a leading and known risk factor for its development. More particularly and despite the underlying mechanisms not being very clear, studies have revealed that the  H. pylori  cytotoxin-associated gene A (CagA) protein plays a key role in this process. In this study it was found that  H. pylori  increased the expression of miR-543 in human gastric cancer tissue when compared with  H. pylori -negative gastric cancer tissue samples. In vitro experiments showed that increased expression of miR-543 induced by CagA is a strong promoter of cell proliferation, migration, and invasion. Conversely, a miR-543 inhibitor suppressed or reversed these effects. It was furthermore found that silencing miR-543 inhibited autophagy and led to epithelial–mesenchymal transition (EMT) under in vitro. The mechanisms by which miR-543 targets SIRT1 to downregulate autophagy was also described. The results suggest that in the progression of  H. pylori -associated gastric cancer, CagA induces overexpression of miR-543, which subsequently targets SIRT1 to suppress autophagy. This may be followed by increased expression of EMT causing cell migration and invasion. Consequently, miR-543 might be considered a therapeutic target for  H. pylori -associated gastric cancer.

SIRT1-targeted miR-543 autophagy inhibition and epithelial–mesenchymal transition promotion in Helicobacter pylori CagA-associated gastric cancer