{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T17:25:00Z","timestamp":1777656300382,"version":"3.51.4"},"reference-count":51,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2011,2,9]],"date-time":"2011-02-09T00:00:00Z","timestamp":1297209600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cancer Science"],"published-print":{"date-parts":[[2011,4]]},"abstract":"<jats:p>Genetic crossing experiments were performed between tuberous sclerosis\u20102 (<jats:italic>Tsc2<\/jats:italic>) KO and expressed in renal carcinoma (<jats:italic>Erc<\/jats:italic>) KO mice to analyze the function of the <jats:italic>Erc<\/jats:italic>\/<jats:italic>mesothelin<\/jats:italic> gene in renal carcinogenesis. We found the number and size of renal tumors were significantly less in <jats:italic>Tsc2<\/jats:italic>+\/\u2212;<jats:italic>Erc<\/jats:italic>\u2212\/\u2212 mice than in <jats:italic>Tsc2<\/jats:italic>+\/\u2212;<jats:italic>Erc<\/jats:italic>+\/+ and <jats:italic>Tsc2<\/jats:italic>+\/\u2212;<jats:italic>Erc<\/jats:italic>+\/\u2212 mice. Tumors from <jats:italic>Tsc2<\/jats:italic>+\/\u2212;<jats:italic>Erc<\/jats:italic>\u2212\/\u2212 mice exhibited reduced cell proliferation and increased apoptosis, as determined by proliferating cell nuclear antigen (Ki67) and TUNEL analysis, respectively. Adhesion to collagen\u2010coated plates <jats:italic>in vitro<\/jats:italic> was enhanced in <jats:italic>Erc<\/jats:italic>\u2010restored cells and decreased in <jats:italic>Erc<\/jats:italic>\u2010suppressed cells with siRNA. Tumor formation by <jats:italic>Tsc2<\/jats:italic>\u2010deficient cells in nude mice was remarkably suppressed by stable knockdown of <jats:italic>Erc<\/jats:italic> with shRNA. Western blot analysis showed that the phosphorylation of focal adhesion kinase, Akt and signal transducer and activator of transcription protein 3 were weaker in <jats:italic>Erc<\/jats:italic>\u2010deficient\/suppressed cells compared with <jats:italic>Erc<\/jats:italic>\u2010expressed cells. These results indicate that deficiency of the <jats:italic>Erc<\/jats:italic>\/<jats:italic>mesothelin<\/jats:italic> gene ameliorates renal carcinogenesis in <jats:italic>Tsc2<\/jats:italic> KO mice and inhibits the phosphorylation of several kinases of cell adhesion mechanism. This suggests that Erc\/mesothelin may have an important role in the promotion and\/or maintenance of carcinogenesis by influencing cell\u2010substrate adhesion via the integrin\u2010related signal pathway. (<jats:italic>Cancer Sci<\/jats:italic> 2011; 102: 720\u2013727)<\/jats:p>","DOI":"10.1111\/j.1349-7006.2011.01846.x","type":"journal-article","created":{"date-parts":[[2011,1,4]],"date-time":"2011-01-04T17:09:42Z","timestamp":1294160982000},"page":"720-727","source":"Crossref","is-referenced-by-count":8,"title":["Deficiency of the <i>Erc<\/i>\/<i>mesothelin<\/i> gene ameliorates renal carcinogenesis in <i>Tsc2<\/i> knockout 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