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    Please use this identifier to cite or link to this item: http://tkuir.lib.tku.edu.tw:8080/dspace/handle/987654321/61771


    Title: The N-terminal domain of EBNA1 acts as a suppressor of the HER2/neu oncogene
    Authors: Liu, Jah-yao;Chuang, Tzu-chao;Way, Tzong-der;Tsai, Tzung-chieh;Hu, Chih-lin;Liu, Guang-yaw;Wang, Shan-shue;Chung, Jing-gung;Kao, Ming-ching
    Contributors: 淡江大學化學學系
    Keywords: HER2/neu;EBV;EBNA1;Cell cycle;Gene therapy
    Date: 2009-01-18
    Issue Date: 2011-10-15 23:38:50 (UTC+8)
    Publisher: Shannon: Elsevier Ireland Ltd
    Abstract: HER2/neu oncogene-mediated malignancy is clearly associated with various human cancers. Therefore, HER2/neu targeting is an effective approach to cancer therapy. We have previously demonstrated that Epstein–Barr virus nuclear antigen-1 (EBNA1) can suppress HER2/neu oncogene expression, although EBNA1 itself has oncogenic potential. Here, we found that the N-terminal domain of EBNA1 alone, named EBNA1-NT, which contains the N-terminal region of amino acid residues 1–86 of EBNA1, is required and sufficient to suppress HER2/neu oncogene expression at the transcriptional level. Furthermore, in EBNA1-NT-transfected HER2/neu-overexpressing cells, we found EBNA1-NT could down-regulate the endogenous production of p185HER2/neu, lower transformation ability, sensitize paclitaxel-induced apoptosis and decrease tumorigenic potential. These data suggest that EBNA1-NT may act as a repressor of the HER2/neu oncogene.
    Relation: Cancer Letters 273(2), pp.273-280
    DOI: 10.1016/j.canlet.2008.08.013
    Appears in Collections:[化學學系暨研究所] 期刊論文

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