Abstract
Abstract Helicobacter pylori infection causes chronic gastric inflammation and peptic ulceration, and is the strongest risk factor for the development of gastric cancer. The cagA (cytotoxin-associated gene A) gene which is one of the most important virulence factors of H. pylori, is believed to contribute to the gastric tissue injury and cancer development. Transforming growth factor-β (TGF-β) signaling plays a pivotal role in modulating gastric mucosal inflammatory responses. Recently, H. pylori infection has been associated with attenuated TGF-β signaling in gastric mucosa. However, the precise underlying mechanism of H. pylori infection on TGF-β signaling and inflammatory response remains unclear. In this study, we examined the mechanism of inhibition of TGF-β signaling by H. pylori CagA protein. CagA suppressed TGF-β/Smad transcriptional responses. CagA interacted constitutively with Smad proteins, and most strongly with Smad3. Expression of CagA on AGS cells inhibited TGF-β-induced down-regulation of proinflammatory chemokines, such as CXCL1, CXCL3 and IL-8, as well as TGF-β-induced transcription of target genes. These results suggest that the attenuated TGF-β signaling associated with cagA-positive H. pylori infection could be an important determinant for the degree of inflammation provoked by H. pylori. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1962. doi:10.1158/1538-7445.AM2011-1962
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