{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T14:34:04Z","timestamp":1790865244042,"version":"4.1.0"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":3471,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2006,3]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>\n                                 <jats:bold>Intrahepatic expression of hepatitis B x antigen (HBxAg) is associated with the development of hepatocellular carcinoma (HCC), perhaps through<\/jats:bold>\n                                 <jats:bold>\n                                    trans\n                                 <\/jats:bold>\n                                 <jats:bold>-activation of selected cellular genes. When this was examined by PowerBlot analysis, upregulated levels of \u03b2-catenin and several known \u03b2-catenin effectors were observed in HBxAg-positive compared with HBxAg-negative HepG2 cells. When HBxAg was introduced into Hep3B cells, upregulated expression of wild-type \u03b2-catenin was observed. This was also observed in Hep3B cells overexpressing the HBxAg upregulated gene, URG11. Upregulated expression of URG11 and \u03b2-catenin correlated with HBxAg<\/jats:bold>\n                                 <jats:bold>\n                                    trans\n                                 <\/jats:bold>\n                                 <jats:bold>-activation function. Transient transfection assays with fragments of the \u03b2-catenin promoter showed that it was activated by both HBxAg and URG11 and inhibited by URG11-specific small inhibitory RNA. The latter also inhibited the growth of Hep3BX cells in a serum-free medium, which correlated with depressed levels of \u03b2-catenin. Activation of \u03b2-catenin effector genes was observed in cells stably expressing HBxAg or overexpressing URG11 compared with control cells transfected with the pTOPFLASH reporter plasmid. Extensive costaining between HBxAg, URG11, and \u03b2-catenin was observed in infected liver and HCC nodules, suggesting a close relationship<\/jats:bold>\n                                 <jats:bold>\n                                    in vivo\n                                 <\/jats:bold>\n                                 <jats:bold>.<\/jats:bold>\n                                 <jats:bold>\n                                    In conclusion\n                                 <\/jats:bold>\n                                 <jats:bold>, wild-type \u03b2-catenin is activated by HBxAg, in part, through the upregulated expression of the HBxAg effector URG11. URG11 stimulates the \u03b2-catenin promoter and hepatocellular growth and survival. These observations also suggest that URG11 may be a regulatory element in the \u03b2-catenin signaling pathway and may be a target for chemoprevention of HCC. (Hepatology 2006;43:415\u2013424.)<\/jats:bold>\n                              <\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.21053","type":"journal-article","created":{"date-parts":[[2006,2,22]],"date-time":"2006-02-22T21:17:19Z","timestamp":1140643039000},"page":"415-424","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":53,"title":["Enhanced cell survival of Hep3B cells by the hepatitis B x antigen effector, URG11, is associated with upregulation of 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