{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T16:45:40Z","timestamp":1790700340722,"version":"4.1.0"},"reference-count":35,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":200,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Hepatology"],"published-print":{"date-parts":[[2015,5]]},"abstract":"<jats:p>\n                    The prognosis for hepatocellular carcinoma (HCC) remains dismal in terms of overall survival (OS), and its molecular pathogenesis has not been completely defined. Here, we report that expression of deubiquitylase ubiquitin\u2010specific protease 7 (USP7) is higher in human HCC tissues than in matched peritumoral tissues. Ectopic USP7 expression promotes growth of HCC cells\n                    <jats:italic toggle=\"yes\">in vivo<\/jats:italic>\n                    and\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    . Mechanistically, USP7 overexpression fosters HCC cell growth by forming a complex with and stabilizing thyroid hormone receptor\u2010interacting protein 12 (TRIP12), which induces constitutive p14\n                    <jats:sup>ARF<\/jats:sup>\n                    ubiquitination. Clinically, USP7 overexpression is significantly correlated with a malignant phenotype, including larger tumor size, multiple tumor, poor differentiation, elevated alpha\u2010fetoprotein, and microvascular invasion. Moreover, overexpression of USP7 and\/or TRIP12 correlates with shorter OS and higher cumulative recurrence rates of HCC.\n                    <jats:italic toggle=\"yes\">Conclusion<\/jats:italic>\n                    : USP7 stabilizes TRIP12 by deubiquitination, thus constitutively inactivating p14\n                    <jats:sup>ARF<\/jats:sup>\n                    and promoting HCC progression. This represents a novel marker for predicting prognosis and a potential therapeutic target for HCC. (H\n                    <jats:sc>epatology<\/jats:sc>\n                    2015;61:1603\u20101614)\n                  <\/jats:p>","DOI":"10.1002\/hep.27682","type":"journal-article","created":{"date-parts":[[2014,12,29]],"date-time":"2014-12-29T13:29:51Z","timestamp":1419859791000},"page":"1603-1614","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":105,"title":["Ubiquitin\u2010specific protease 7 accelerates p14ARF degradation by deubiquitinating thyroid hormone receptor\u2010interacting protein 12 and promotes hepatocellular carcinoma progression"],"prefix":"10.1097","volume":"61","author":[{"given":"Jia\u2010Bin","family":"Cai","sequence":"first","affiliation":[{"name":"Liver Cancer Institute, Zhongshan Hospital,Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of 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Education,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong\u2010Hui","family":"Ma","sequence":"additional","affiliation":[{"name":"Laboratory of Epigenetics,Institutes of Biomedical Sciences, Fudan University,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiang","family":"Gao","sequence":"additional","affiliation":[{"name":"Liver Cancer Institute, Zhongshan Hospital,Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zao\u2010Zhuo","family":"Shen","sequence":"additional","affiliation":[{"name":"Liver Cancer Institute, Zhongshan Hospital,Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of 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University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peng\u2010Fei","family":"Zhang","sequence":"additional","affiliation":[{"name":"Liver Cancer Institute, Zhongshan Hospital,Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chi","family":"Zhang","sequence":"additional","affiliation":[{"name":"Liver Cancer Institute, Zhongshan Hospital,Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mei\u2010Yu","family":"Hu","sequence":"additional","affiliation":[{"name":"Liver Cancer Institute, Zhongshan Hospital,Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liu\u2010Xiao","family":"Yang","sequence":"additional","affiliation":[{"name":"Liver Cancer Institute, Zhongshan Hospital,Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying\u2010Hong","family":"Shi","sequence":"additional","affiliation":[{"name":"Liver Cancer Institute, Zhongshan Hospital,Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education,Shanghai,China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao\u2010Ying","family":"Wang","sequence":"additional","affiliation":[{"name":"Liver Cancer Institute, Zhongshan Hospital,Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of 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