English  |  正體中文  |  简体中文  |  Items with full text/Total items : 16714/19009 (88%)
Visitors : 5703820      Online Users : 54
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/27607


    標題: Endoplasmic Reticulum Stress Stimulates p53 Expression through NF-kappa B Activation
    作者: Lin, Wan-Chi
    Chuang, Yu-Chi
    Chang, Yung-Sheng
    Lai, Ming-Derg
    Teng, Yen-Ni
    Su, Ih-Jen
    Wang, Clay C.C.
    Lee, Kuan-Han
    Hung, Jui-Hsiang
    Su, Ih-Jen�
    貢獻者: 藥學系
    生物科技系
    關鍵字: Unfolded Protein Response
    Glycogen-Synthase Kinase-3-Beta
    Transcription Factor
    Induced Apoptosis
    Transmembrane Protein
    Messenger-Rna
    Dna-Damage
    Er Stress
    Phosphorylation
    Kinase
    日期: 2012-07-30
    上傳時間: 2014-03-21 16:15:04 (UTC+8)
    出版者: Public Library Science
    摘要: Background: Induction of apoptosis by endoplasmic reticulum (ER) stress is implicated as the major factor in the development of multiple diseases. ER stress also appears to be a potentially useful major response to many chemotherapeutic drugs and environmental chemical compounds. A previous study has indicated that one major apoptotic regulator, p53, is significantly increased in response to ER stress, and participates in ER stress-induced apoptosis. However, the regulators of p53 expression during ER stress are still not fully understood.Principal Findings: In this report, we demonstrate that induction of p53 expression is mediated through NF-kappa B signaling pathways during ER stress in MCF-7 cells. Tunicamycin or brefeldin A, two ER stress inducers, increased p53 expression in MCF-7 and Hela cells. We found p53 nuclear localization, activity, and phosphorylation at serine 15 on p53 increased during ER stress. Nuclear translocation of NF-kappa B and activity of NF-kappa B were also observed during ER stress. ER stress-induced p53 expression was significantly inhibited by coincubation with the NF-kappa B inhibitor, Bay 11-7082 and downregulation of NF-kappa B p65 expression. The role of p53 in mediating Brefeldin A-induced apoptosis was also investigated. Induction of p53 expression by Brefeldin A was correlated to Brefeldin A-induced apoptosis. Furthermore, downregulation of p53 expression by p53 siRNA significantly reduced Brefeldin A-induced apoptosis in MCF-7 cells.Significance: Taken together, NF-kappa B activation and induction of p53 expression is essential for ER stress-induced cell death which is important for therapeutic effects of clinical cancer drugs. Our results may provide insight into the mechanism of cancer chemotherapy efficacy that is associated with induction of ER stress.
    關聯: Plos One, 7(7), e39120
    Appears in Collections:[藥學系(所)] 期刊論文
    [生物科技系(所)] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML265View/Open


    All items in CNU IR are protected by copyright, with all rights reserved.


    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback