Recoding RNA editing of AZIN1 predisposes to hepatocellular carcinoma View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2013-02

AUTHORS

Leilei Chen, Yan Li, Chi Ho Lin, Tim Hon Man Chan, Raymond Kwok Kei Chow, Yangyang Song, Ming Liu, Yun-Fei Yuan, Li Fu, Kar Lok Kong, Lihua Qi, Yan Li, Na Zhang, Amy Hin Yan Tong, Dora Lai-Wan Kwong, Kwan Man, Chung Mau Lo, Si Lok, Daniel G Tenen, Xin-Yuan Guan

ABSTRACT

A 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. More... »

PAGES

209

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nm.3043

    DOI

    http://dx.doi.org/10.1038/nm.3043

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1019532053

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/23291631


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