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Article: Recoding RNA editing of AZIN1 predisposes to hepatocellular carcinoma

TitleRecoding RNA editing of AZIN1 predisposes to hepatocellular carcinoma
Authors
Issue Date2013
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nm
Citation
Nature Medicine, 2013, v. 19 n. 2, p. 209-216 How to Cite?
AbstractA better understanding of human hepatocellular carcinoma (HCC) pathogenesis at the molecular level will facilitate the discovery of tumor-initiating events. Transcriptome sequencing revealed that adenosine-to-inosine (A→I) RNA editing of AZIN1 (encoding antizyme inhibitor 1) is increased in HCC specimens. A→I editing of AZIN1 transcripts, specifically regulated by ADAR1 (encoding adenosine deaminase acting on RNA-1), results in a serine-to-glycine substitution at residue 367 of AZIN1, located in β-strand 15 (β15) and predicted to cause a conformational change, induced a cytoplasmic-to-nuclear translocation and conferred gain-of-function phenotypes that were manifested by augmented tumor-initiating potential and more aggressive behavior. Compared with wild-type AZIN1 protein, the edited form has a stronger affinity to antizyme, and the resultant higher AZIN1 protein stability promotes cell proliferation through the neutralization of antizyme-mediated degradation of ornithine decarboxylase (ODC) and cyclin D1 (CCND1). Collectively, A→I RNA editing of AZIN1 may be a potential driver in the pathogenesis of human cancers, particularly HCC. © 2013 Nature America, Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/181977
ISSN
2015 Impact Factor: 30.357
2015 SCImago Journal Rankings: 13.959
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChen, L-
dc.contributor.authorLi, Y-
dc.contributor.authorLin, C-
dc.contributor.authorChan, HM-
dc.contributor.authorChow, KK-
dc.contributor.authorSong, Y-
dc.contributor.authorLiu, M-
dc.contributor.authorYuan, YF-
dc.contributor.authorFu, L-
dc.contributor.authorKong, KL-
dc.contributor.authorQi, L-
dc.contributor.authorLi, Y-
dc.contributor.authorZhang, N-
dc.contributor.authorTong, AHY-
dc.contributor.authorKwong, DLW-
dc.contributor.authorMan, K-
dc.contributor.authorLo, CM-
dc.contributor.authorLok, S-
dc.contributor.authorTenen, DG-
dc.contributor.authorGuan, X-
dc.date.accessioned2013-04-17T07:15:59Z-
dc.date.available2013-04-17T07:15:59Z-
dc.date.issued2013-
dc.identifier.citationNature Medicine, 2013, v. 19 n. 2, p. 209-216-
dc.identifier.issn1078-8956-
dc.identifier.urihttp://hdl.handle.net/10722/181977-
dc.description.abstractA better understanding of human hepatocellular carcinoma (HCC) pathogenesis at the molecular level will facilitate the discovery of tumor-initiating events. Transcriptome sequencing revealed that adenosine-to-inosine (A→I) RNA editing of AZIN1 (encoding antizyme inhibitor 1) is increased in HCC specimens. A→I editing of AZIN1 transcripts, specifically regulated by ADAR1 (encoding adenosine deaminase acting on RNA-1), results in a serine-to-glycine substitution at residue 367 of AZIN1, located in β-strand 15 (β15) and predicted to cause a conformational change, induced a cytoplasmic-to-nuclear translocation and conferred gain-of-function phenotypes that were manifested by augmented tumor-initiating potential and more aggressive behavior. Compared with wild-type AZIN1 protein, the edited form has a stronger affinity to antizyme, and the resultant higher AZIN1 protein stability promotes cell proliferation through the neutralization of antizyme-mediated degradation of ornithine decarboxylase (ODC) and cyclin D1 (CCND1). Collectively, A→I RNA editing of AZIN1 may be a potential driver in the pathogenesis of human cancers, particularly HCC. © 2013 Nature America, Inc. All rights reserved.-
dc.languageeng-
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/nm-
dc.relation.ispartofNature Medicine-
dc.titleRecoding RNA editing of AZIN1 predisposes to hepatocellular carcinoma-
dc.typeArticle-
dc.identifier.emailChen, L: pollyllc@hku.hk-
dc.identifier.emailLi, Y: vikkiyan@hku.hk-
dc.identifier.emailLin, C: nicklin@hku.hk-
dc.identifier.emailChan, HM: chantim@hkucc.hku.hk-
dc.identifier.emailChow, KK: raymchow@hku.hk-
dc.identifier.emailFu, L: gracefu@graduate.hku.hk-
dc.identifier.emailKong, KL: karlok@hku.hk-
dc.identifier.emailZhang, N: zhangna@hku.hk-
dc.identifier.emailKwong, DLW: dlwkwong@hku.hk-
dc.identifier.emailMan, K: kwanman@hku.hk-
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hk-
dc.identifier.emailLok, S: silok@genome.hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.authorityFu, L=rp01435-
dc.identifier.authorityKwong, DLW=rp00414-
dc.identifier.authorityMan, K=rp00417-
dc.identifier.authorityLo, CM=rp00412-
dc.identifier.authorityLok, S=rp00271-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.doi10.1038/nm.3043-
dc.identifier.pmid23291631-
dc.identifier.scopuseid_2-s2.0-84873531277-
dc.identifier.hkuros213809-
dc.identifier.volume19-
dc.identifier.issue2-
dc.identifier.spage209-
dc.identifier.epage216-
dc.identifier.isiWOS:000314675900029-
dc.publisher.placeUnited States-

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