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    MiR-196a exerts its oncogenic effect in glioblastoma multiforme by inhibition of IκBα both in vitro and in vivo

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    Type
    Article
    Authors
    Yang, Guang
    Han, Dayong
    Chen, Xin
    Zhang, Daming
    Wang, Lu
    Shi, Chen
    Zhang, Weiguang
    Li, Chenguang
    Chen, Xiaofeng
    Liu, Huailei
    Zhang, Dongzhi
    Kang, Jianhao
    Peng, Fei
    Liu, Ziyi
    Qi, Jiping
    Gao, Xin cc
    Ai, Jing
    Shi, Changbin
    Zhao, Shiguang
    KAUST Department
    Computer, Electrical and Mathematical Sciences and Engineering (CEMSE) Division
    Computer Science Program
    Computational Bioscience Research Center (CBRC)
    Structural and Functional Bioinformatics Group
    Date
    2014-01-23
    Online Publication Date
    2014-01-23
    Print Publication Date
    2014-05
    Permanent link to this record
    http://hdl.handle.net/10754/563351
    
    Metadata
    Show full item record
    Abstract
    BackgroundRecent studies have revealed that miR-196a is upregulated in glioblastoma multiforme (GBM) and that it correlates with the clinical outcome of patients with GBM. However, its potential regulatory mechanisms in GBM have never been reported.MethodsWe used quantitative real-time PCR to assess miR-196a expression levels in 132 GBM specimens in a single institution. Oncogenic capability of miR-196a was detected by apoptosis and proliferation assays in U87MG and T98G cells. Immunohistochemistry was used to determine the expression of IκBα in GBM tissues, and a luciferase reporter assay was carried out to confirm whether IκBα is a direct target of miR-196a. In vivo, xenograft tumors were examined for an antiglioma effect of miR-196a inhibitors.ResultsWe present for the first time evidence that miR-196a could directly interact with IκBα 3′-UTR to suppress IκBα expression and subsequently promote activation of NF-κB, consequently promoting proliferation of and suppressing apoptosis in GBM cells both in vitro and in vivo. Our study confirmed that miR-196a was upregulated in GBM specimens and that high levels of miR-196a were significantly correlated with poor outcome in a large cohort of GBM patients. Our data from human tumor xenografts in nude mice treated with miR-196 inhibitors demonstrated that inhibition of miR-196a could ameliorate tumor growth in vivo.ConclusionsMiR-196a exerts its oncogenic effect in GBM by inhibiting IκBα both in vitro and in vivo. Our findings provide new insights into the pathogenesis of GBM and indicate that miR-196a may predict clinical outcome of GBM patients and serve as a new therapeutic target for GBM. © 2014 © The Author(s) 2014. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
    Citation
    Yang, G., Han, D., Chen, X., Zhang, D., Wang, L., Shi, C., … Zhao, S. (2014). MiR-196a exerts its oncogenic effect in glioblastoma multiforme by inhibition of IκBα both in vitro and in vivo. Neuro-Oncology, 16(5), 652–661. doi:10.1093/neuonc/not307
    Sponsors
    This work was supported by National Natural Science Foundations of China [81302178; 81272788]; Natural Science Foundations of Heilongjiang [QC2013C096]; the Fund of the First Affiliated Hospital of Harbin Medical University [2013B01].
    Publisher
    Oxford University Press (OUP)
    Journal
    Neuro-Oncology
    DOI
    10.1093/neuonc/not307
    PubMed ID
    24463357
    PubMed Central ID
    PMC3984554
    Additional Links
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3984554
    ae974a485f413a2113503eed53cd6c53
    10.1093/neuonc/not307
    Scopus Count
    Collections
    Articles; Structural and Functional Bioinformatics Group; Computer Science Program; Computational Bioscience Research Center (CBRC); Computer, Electrical and Mathematical Science and Engineering (CEMSE) Division

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