| [ Summary ] |
Recent studies have shown that Helicobacter pylori (H. pylori) cagA-positive strains play an essential role in the development of gastric carcinoma. The cagA-encoded virulence factor CagA is delivered into H. pylori-attached gastric epithelial cells via the bacterial syringe-like apparatus termed the type Ⅳ secretion system (TFSS). In gastric epithelial cells, injected CagA interacts with a number of cell-signaling molecules, most notably SHP-2 phosphatase and PAR1b kinase, that are involved in the regulation of cell proliferation, cell motility and cell polarity. As a result, CagA causes cellular dysfunction that leads to transformation of gastric epithelial cells. Transgenic mice that systemically express the CagA protein develop gastrointestinal and hematological malignancies. These observations provide strong evidence that H. pylori CagA is the bacterial oncoprotein which plays a crucial role in the H. pylori-mediated gastric carcinogenesis. |