IGF-II induced by hepatitis B virus X protein regulates EMT via SUMO mediated loss of E- cadherin in mice

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dc.contributor.authorHye-Lin Ha-
dc.contributor.authorTaeho Kwon-
dc.contributor.authorIn Seon Bak-
dc.contributor.authorR L Erikson-
dc.contributor.authorBo Yeon Kim-
dc.contributor.authorDae Yeul Yu-
dc.date.accessioned2017-04-19T10:30:09Z-
dc.date.available2017-04-19T10:30:09Z-
dc.date.issued2016-
dc.identifier.issn19492553-
dc.identifier.uri10.18632/oncotarget.10922ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/13543-
dc.description.abstractHepatocellular carcinoma (HCC) is one of the most common cancers and a leading cause of cancer mortality. Prognosis of this disease largely depends on its stage. An Enlarged liver, due to dysplasia, may be a critical point in the multi-step progression to HCC. The mechanism underlying hepatomegaly in human and mouse models are poorly understood. We previously reported we observed enlarged liver in hepatitis B virus X protein (HBx) expressing mice (HBx mice). Here we identify the critical role of HBx induced IGF-II in hepatomegaly in mice and abnormal cell growth in human hepatoma cells. We found that HBx induced IGF-II is essential to induce epithelial-mesenchymal transition (EMT) through loss of E-cadherin. In mouse liver, loss of E-cadherin was mediated by post-translational regulation, at least in part, by protease and SUMOylation not by transcriptional regulation. In contrast, in hepatoma cell line (HepG2 cells) Akt signal pathway controls the mRNA expression level of EMT-related transcription factors, especially Twist, in addition to post- translational modification through SUMOylation. Thus, IGF-II-mediated loss of E-cadherin is central in developing hepatomegaly in mice and abnormal cell growth in the hepatoma cell line. HBx induced IGF-II represents a potential biomarker, which is also a therapeutic target in HCC.-
dc.publisherImpact Journalsko
dc.titleIGF-II induced by hepatitis B virus X protein regulates EMT via SUMO mediated loss of E- cadherin in mice-
dc.title.alternativeIGF-II induced by hepatitis B virus X protein regulates EMT via SUMO mediated loss of E- cadherin in mice-
dc.typeArticle-
dc.citation.titleOncotarget-
dc.citation.number35-
dc.citation.endPage56957-
dc.citation.startPage56944-
dc.citation.volume7-
dc.contributor.affiliatedAuthorTaeho Kwon-
dc.contributor.affiliatedAuthorBo Yeon Kim-
dc.contributor.alternativeName하혜린-
dc.contributor.alternativeName권태호-
dc.contributor.alternativeName박인선-
dc.contributor.alternativeNameErikson-
dc.contributor.alternativeName김보연-
dc.contributor.alternativeName유대열-
dc.identifier.bibliographicCitationOncotarget, vol. 7, no. 35, pp. 56944-56957-
dc.identifier.doi10.18632/oncotarget.10922-
dc.subject.keywordEpithelial-mesenchymal transition-
dc.subject.keywordHepatitis B virus X protein-
dc.subject.keywordHepatocellular carcinoma-
dc.subject.keywordIGF-II-
dc.subject.keywordSUMOylation-
dc.subject.localEpithelial-mesenchymal transition-
dc.subject.localEpithelial-mesenchymal transition (EMT)-
dc.subject.localHepatitis B virus X protein-
dc.subject.localHepatocellular carcinoma-
dc.subject.localHepatocellular carcinoma (HCC)-
dc.subject.localIGF-II-
dc.subject.localSUMOylation-
dc.description.journalClassN-
Appears in Collections:
Jeonbuk Branch Institute > Primate Resources Center > 1. Journal Articles
Ochang Branch Institute > Anticancer Agent Research Center > 1. Journal Articles
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