Please use this identifier to cite or link to this item: https://doi.org/10.1093/nar/gky396
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dc.titleBidirectional regulation of adenosine-to-inosine (A-to-I) RNA editing by DEAH box helicase 9 (DHX9) in cancer
dc.contributor.authorHong, HuiQi
dc.contributor.authorAn, Omer
dc.contributor.authorChan, Tim HM
dc.contributor.authorNg, Vanessa HE
dc.contributor.authorKwok, Hui Si
dc.contributor.authorLin, Jaymie S
dc.contributor.authorQi, Lihua
dc.contributor.authorHan, Jian
dc.contributor.authorTay, Daryl JT
dc.contributor.authorTang, Sze Jing
dc.contributor.authorYang, Henry
dc.contributor.authorSong, Yangyang
dc.contributor.authorMolias, Fernando Bellido
dc.contributor.authorTenen, Daniel G
dc.contributor.authorChen, Leilei
dc.date.accessioned2019-06-07T01:34:33Z
dc.date.available2019-06-07T01:34:33Z
dc.date.issued2018-09-06
dc.identifier.citationHong, HuiQi, An, Omer, Chan, Tim HM, Ng, Vanessa HE, Kwok, Hui Si, Lin, Jaymie S, Qi, Lihua, Han, Jian, Tay, Daryl JT, Tang, Sze Jing, Yang, Henry, Song, Yangyang, Molias, Fernando Bellido, Tenen, Daniel G, Chen, Leilei (2018-09-06). Bidirectional regulation of adenosine-to-inosine (A-to-I) RNA editing by DEAH box helicase 9 (DHX9) in cancer. NUCLEIC ACIDS RESEARCH 46 (15) : 7953-7969. ScholarBank@NUS Repository. https://doi.org/10.1093/nar/gky396
dc.identifier.issn0305-1048
dc.identifier.issn1362-4962
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/155274
dc.description.abstract© The Author(s) 2018. Published by Oxford University Press on behalf of Nucleic Acids Research. Adenosine-to-inosine (A-to-I) RNA editing entails the enzymatic deamination of adenosines to inosines by adenosine deaminases acting on RNA (ADARs). Dysregulated A-to-I editing has been implicated in various diseases, including cancers. However, the precise factors governing the A-to-I editing and their physiopathological implications remain as a longstanding question. Herein, we unravel that DEAH box helicase 9 (DHX9), at least partially dependent of its helicase activity, functions as a bidirectional regulator of A-to-I editing in cancer cells. Intriguingly, the ADAR substrate specificity determines the opposing effects of DHX9 on editing as DHX9 silencing preferentially represses editing of ADAR1-specific substrates, whereas augments ADAR2-specific substrate editing. Analysis of 11 cancer types from The Cancer Genome Atlas (TCGA) reveals a striking overexpression of DHX9 in tumors. Further, tumorigenicity studies demonstrate a helicase-dependent oncogenic role of DHX9 in cancer development. In sum, DHX9 constitutes a bidirectional regulatory mode in A-to-I editing, which is in part responsible for the dysregulated editome profile in cancer.
dc.language.isoen
dc.publisherOXFORD UNIV PRESS
dc.sourceElements
dc.subjectScience & Technology
dc.subjectLife Sciences & Biomedicine
dc.subjectBiochemistry & Molecular Biology
dc.subjectPRE-MESSENGER-RNA
dc.subjectGLUTAMATE-RECEPTOR SUBUNITS
dc.subjectHEPATOCELLULAR-CARCINOMA
dc.subjectGENETIC-VARIATION
dc.subjectREAD ALIGNMENT
dc.subjectPOLYMERASE-II
dc.subjectHUMAN-CELLS
dc.subjectDEAMINASES
dc.subjectADAR
dc.subjectDATABASE
dc.typeArticle
dc.date.updated2019-06-03T09:34:26Z
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.1093/nar/gky396
dc.description.sourcetitleNUCLEIC ACIDS RESEARCH
dc.description.volume46
dc.description.issue15
dc.description.page7953-7969
dc.published.statePublished
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