{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,31]],"date-time":"2023-10-31T06:47:42Z","timestamp":1698734862079},"reference-count":22,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2012,3,8]],"date-time":"2012-03-08T00:00:00Z","timestamp":1331164800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Helicobacter"],"published-print":{"date-parts":[[2012,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>Background and Aims:\u2002<\/jats:bold> Infection by <jats:italic>Helicobacter pylori<\/jats:italic> is one of the major contributing factors of chronic active gastritis and peptic ulcer and is closely associated with the occurrence and progression of gastric cancer. CagA protein is a major virulence factor of <jats:italic>H. pylori<\/jats:italic> that interacts with SHP\u20102, a true oncogene, to interfere with cellular signaling pathways; CagA also plays a crucial role in promoting the carcinogenesis of gastric epithelial cells. However, currently, the molecular mechanisms of gastric epithelial cells that antagonize CagA pathogenesis remain inconclusive.<\/jats:p><jats:p><jats:bold>Methods:\u2002<\/jats:bold> We showed that AGS gastric cancer cells transfected with CagA exhibited the inhibition of proliferation and increased activity of caspase 3\/7 using two\u2010dimensional gel electrophoresis and secondary mass spectrometry (MS\/MS).<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> It was found that the AGS gastric cancer cells stably expressing CagA displayed significantly increased the expression of 16 proteins, including hnRNPC1\/2. Further analysis revealed that hnRNPC1\/2 significantly boosted the expression of the p27<jats:sup>kip1<\/jats:sup> protein.<\/jats:p><jats:p><jats:bold>Conclusion:<\/jats:bold> Our data suggested that hnRNPC1\/2 upregulates p27<jats:sup>kip1<\/jats:sup> expression and the subsequent suppression of cell proliferation and induction of apoptosis, thereby providing an important mechanism whereby gastric epithelial cells antagonize CagA\u2010mediated pathogenesis.<\/jats:p>","DOI":"10.1111\/j.1523-5378.2011.00927.x","type":"journal-article","created":{"date-parts":[[2012,3,8]],"date-time":"2012-03-08T15:06:35Z","timestamp":1331219195000},"page":"140-147","source":"Crossref","is-referenced-by-count":0,"title":["p27<sup>kip1<\/sup> Upregulated by hnRNPC1\/2 Antagonizes CagA (a Virulence Factor of <i>Helicobacter pylori<\/i>)\u2010Mediated Pathogenesis"],"prefix":"10.1111","volume":"17","author":[{"given":"Shenghang","family":"Jin","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Minjin","family":"Wu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hanqin","family":"Cao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sunke","family":"Ying","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jiping","family":"Hua","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yu","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2012,3,8]]},"reference":[{"key":"e_1_2_6_2_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10552-010-9707-2"},{"key":"e_1_2_6_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.idc.2010.07.010"},{"key":"e_1_2_6_4_2","doi-asserted-by":"publisher","DOI":"10.1097\/MOG.0b013e32833efede"},{"key":"e_1_2_6_5_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.222375399"},{"key":"e_1_2_6_6_2","doi-asserted-by":"crossref","first-page":"14559","DOI":"10.1073\/pnas.96.25.14559","article-title":"Altered 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