MicroRNA-146a Enhances Helicobacter pylori Induced Cell Apoptosis in Human Gastric Cancer Cells

About 50% of the world’s population is infected with Helicobacter pylori (H. pylori), which is a causative agent for gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric cancer (Salama et al., 2013). It is estimated that individuals infected with H. pylori have more than two-fold increased risk of developing gastric cancer compared with noninfected ones (Brenner et al., 2000) and nearly all gastric cancer is related to H. pylori (Uemura et al., 2000). Why only 1 to 5% of H. pylori infected persons develop gastric cancer remains unknown and it seems to depend on the relationship between environmental, bacterial virulence factors and host genetics. As a type of cellular suicide, apoptosis occurs in single cells, in response to the expression of specific cellular genes. Tissue integrity is maintained when the rate of cell loss by apoptosis is matched by the rate of new cell production by proliferation. For this reason, apoptosis was considered as a mechanism to block tumor formation. It has been demonstrated that H. pylori infection is crucial in disturbed regulation of epithelial cell apoptosis and may therefore link the multistep process of carcinogenesis (Targosz et al., 2012). However, the regulatory mechanism of H. pylori-induced apoptosis in gastric cancer cells is still not well understood. The human transcriptome comprises not only large numbers of protein-coding messenger RNAs (mRNAs),