{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T01:18:41Z","timestamp":1792631921892,"version":"4.5.0"},"reference-count":52,"publisher":"Baishideng Publishing Group Inc.","issue":"41","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["World J Gastroenterol"],"abstract":"<jats:p>BACKGROUND<\/jats:p>\n          <jats:p>Helicobacter pylori  (H. pylori ) persistently colonizes the human gastric mucosa in more than 50% of the global population, leading to various gastroduodenal diseases ranging from chronic gastritis to gastric carcinoma. Cytotoxin-associated gene A (CagA) protein, an important oncoprotein, has highly polymorphic Glu-Pro-Ile-Tyr-Ala segments at the carboxyl terminus, which play crucial roles in pathogenesis. Our previous study revealed a significant association between amino acid deletions at positions 893 and 894 and gastric cancer.<\/jats:p>\n          <jats:p>AIM<\/jats:p>\n          <jats:p>To investigate the impact of amino acid deletions at positions 893 and 894 on CagA function.<\/jats:p>\n          <jats:p>METHODS<\/jats:p>\n          <jats:p>We selected a representative HZT strain from a gastric cancer patient with amino acid deletions at positions 893 and 894. The cagA  gene was amplified and mutated into cagA -NT and cagA -NE (sequence characteristics of strains from nongastric cancer patients), cloned and inserted into pAdtrack-CMV, and then transfected into AGS cells. The expression of cagA  and its mutants was examined using real-time polymerase chain reaction and Western blotting, cell elongation via  cell counting, F-actin cytoskeleton visualization using fluorescence staining, and interleukin-8 (IL-8) secretion via  enzyme-linked immunosorbent assay.<\/jats:p>\n          <jats:p>RESULTS<\/jats:p>\n          <jats:p>The results revealed that pAdtrack\/cagA  induced a more pronounced hummingbird phenotype than pAdtrack\/cagA -NT and pAdtrack\/cagA -NE (40.88 \u00b1 3.10 vs  32.50 \u00b1 3.17, P  &lt; 0.001 and 40.88 \u00b1 3.10 vs  32.17 \u00b1 3.00, P  &lt; 0.001) at 12 hours after transfection. At 24 hours, pAdtrack\/cagA- NE induced significantly fewer hummingbird phenotypes than pAdtrack\/cagA  and pAdtrack\/cagA- NT (46.02 \u00b1 2.12 vs  53.90 \u00b1 2.10, P  &lt; 0.001 and 46.02 \u00b1 2.12 vs  51.15 \u00b1 3.74, P  &lt; 0.001). The total amount of F-actin caused by pAdtrack\/cagA  was significantly lower than that caused by pAdtrack\/cagA- NT and pAdtrack\/cagA- NE (27.54 \u00b1 17.37 vs  41.51 \u00b1 11.90, P  &lt; 0.001 and 27.54 \u00b1 17.37 vs  41.39 \u00b1 14.22, P  &lt; 0.001) at 12 hours after transfection. Additionally, pAdtrack\/cagA  induced higher IL-8 secretion than pAdtrack\/cagA- NT and pAdtrack\/cagA- NE at different times after transfection.<\/jats:p>\n          <jats:p>CONCLUSION<\/jats:p>\n          <jats:p>Amino acid deletions at positions 893 and 894 enhance CagA pathogenicity, which is crucial for revealing the pathogenic mechanism of CagA and identifying biomarkers of highly pathogenic H. pylori .<\/jats:p>","DOI":"10.3748\/wjg.v30.i41.4449","type":"journal-article","created":{"date-parts":[[2024,10,23]],"date-time":"2024-10-23T02:18:31Z","timestamp":1729649911000},"page":"4449-4460","source":"Crossref","is-referenced-by-count":4,"title":["Amino acid deletions at positions 893 and 894 of cytotoxin-associated gene A protein affect <i>Helicobacter pylori<\/i> gastric epithelial cell 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