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Helicobacter pylori CagA and gastric carcinogenesis. | LitMetric

Helicobacter pylori CagA and gastric carcinogenesis.

Asian Pac J Cancer Prev

Department of Gastroenterology, Yanda International Hospital, East Beijing, China.

Published: October 2014

AI Article Synopsis

  • The study aimed to explore the structure and activity of the CagA gene from Helicobacter pylori with a focus on tyrosine phosphorylation motifs and its interaction with SHP-2 in relation to gastric cancer.
  • Sixteen H. pylori strains from patients with either duodenal ulcers or gastric adenocarcinoma were analyzed for their CagA characteristics, with results showing nearly universal expression and activity of CagA across strains.
  • Although CagA was more expressed in gastric adenocarcinoma patients, the structural features of the CagA gene showed no significant differences between the two patient groups.

Article Abstract

Objectives: This study aimed to demonstrate the tyrosine phosphorylation motif (TPM) and 3' region structure of the Helicobacter pylori CagA gene as well as its SHP-2 binding activity in AGS cells and relation to gastric carcinogenesis.

Methods: Sixteen clinical isolate H. pylori strains from eight duodenal ulcer and eight gastric adenocarcinoma patients were studied for CagA repeat sequence EPIYA motifs, C-terminal structure, and western blot analysis of CagA protein expression, translocation, and SHP-2 binding in AGS cells.

Results: Except for strain 547, all strains from the gastric adenocarcinoma patients were positive for CagA by PCR and had three EPIYA copy motifs. Western blotting showed that all strains were positive for CagA protein expression (100%), CagA protein translocation (100%), and SHP-2 binding (100%). CagA protein expression was significantly higher in the gastric adenocarcinoma patients than in the duodenal ulcer patients (P=0.0023). CagA protein translocation and SHP-2 binding in the gastric adenocarcinoma patients were higher than those in the duodenal ulcer patients, but no significant differences were found between the two groups (P=0.59, P=0.21, respectively).

Conclusions: The TPMs and 3' region structures of the H. pylori CagA gene in the duodenal ulcer and gastric adenocarcinoma patients have no significant differences.

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Source
http://dx.doi.org/10.7314/apjcp.2012.13.12.6305DOI Listing

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