Abstract
Helicobacter pylori (H. pylori) infection induces apoptosis in gastric epithelial cells, and this occurrence may link to gastric carcinogenesis. However, the regulatory mechanism of H. pylori-induced apoptosis is not clear. MicroRNA-146a has been implicated as a key regulator of the immune system. This report describes our discovery of molecular mechanisms of microRNA-146a regulation of apoptosis in human gastric cancer cells. We found that overexpression of microRNA-146a by transfecting microRNA-146a mimics could significantly enhance apoptosis, and this up-regulation was triggered by COX-2 inhibition. Furthermore, we found that microRNA-146a density was positively correlated with apoptosis rates in H. pylori-positive gastric cancer tissues and intratumoral microRNA-146a density was negatively correlated with lymph node metastasis among H. pylori-positive gastric cancer patients. Understanding the important roles of microRNA-146a in regulating cell apoptosis in H. pylori infected human gastric cancer cells will contribute to the development of microRNA targeted therapy in the future.
Highlights
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)
We found that microRNA-146a density was positively correlated with apoptosis rates in H. pylori-positive gastric cancer tissues and intratumoral microRNA-146a density was negatively correlated with lymph node metastasis among H. pylori-positive gastric cancer patients
Using the H. pylori infected MKN7 cell model, we found that expression of microRNA-146a (Figure 1A) and cell apoptosis (Figure 1B) were enhanced simultaneously under H. pylori infection (p
Summary
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). 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. 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. The regulatory mechanism of H. pylori-induced apoptosis in gastric cancer cells is still not well understood
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