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题目:: Recoding RNA editing of AZIN1 predisposes to hepatocellular carcinoma.
作者:: Chen(Leilei),Li(Yan),Lin(Chi Ho),Chan(Tim Hon Man),Chow(Raymond Kwok Kei),Song(Yangyang),Liu(Ming),Yuan(Yun-Fei),Fu(Li),Kong(Kar Lok),Qi(Lihua),Li(Yan),Zhang(Na),Tong(Amy Hin Yan),Kwong(Dora Lai-Wan),Man(Kwan),Lo(Chung Mau),Lok(Si),Tenen(Daniel G),Guan(Xin-Yuan)
状态:: 发布时间2013-02-07 , 更新时间 2016-10-25
期刊:: Nat Med
摘要:: 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.
语言:: eng
DOI:

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