Analysis of correlation between HP infection and activation of PI3K/Akt pathway in mucosal tissues of gastric cancer and precancerous lesions
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- Published online on: August 20, 2018 https://doi.org/10.3892/ol.2018.9329
- Pages: 5615-5620
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Copyright: © Xie et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Abstract
The aim of the study was to investigate the correlation between Helicobacter pylori (HP) infection and activation of the phosphatidylinositol-3-kinase/Akt (PI3K/Akt) pathway in mucosal tissues of gastric cancer and precancerous lesions. Patients with chronic atrophic gastritis (n=52) and gastric cancer (n=98) were treated in the Department of Gastroenterology at The Fifth People's Hospital of Chongqing from August 2011 to August 2016 were selected, and the biopsy tissue and serum specimens were collected. The HP infection was detected via enzyme-linked immunosorbent assay (ELISA), and the expression level of phosphorylated-Akt (p-Akt) was detected via immunohistochemistry (IHC). Moreover, in vivo experiments were performed to simulate HP infection in gastric cancer cells (MGC-803 and AGS), and the p-Akt protein level, PI3K activity and cell proliferative activity were detected. Finally, the changes in Akt protein level were detected by co-culture of gastric cancer cells via LY294002, a PI3K inhibitor, and HP. The positive rate of HP infection in patients with chronic atrophic gastritis was 84.6% (44/52), which was significantly higher than that in patients with gastric cancer [73.5% (72/98)] (p<0.05). The positive rate of HP infection in patients with early gastric cancer (86.4%) was significantly higher than that in patients with moderate-advanced gastric cancer (69.7%) (p<0.05). Results of IHC and western blot analysis revealed that the p-Akt expression level in HP-positive tissues was obviously higher than that in HP-negative tissues (p<0.05). In vitro cell experiments revealed that the PI3K activity was enhanced and the PI3K/Akt pathway was significantly activated after HP infection in tumor cells, thus promoting the proliferation of tumor cells (p<0.05) in a time-dependent manner. After LY294002 inhibited PI3K activity, Akt was not significantly activated by HP infection. Thus, HP activates the PI3K/Akt pathway in gastric cancer cells, thereby promoting tumor cell proliferation.
