國家衛生研究院 NHRI:Item 3990099045/2752
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12500/13673 (91%)
造访人次 : 2475555      在线人数 : 108
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧:
  • 您可在西文检索词汇前后加上"双引号",以获取较精准的检索结果
  • 若欲以作者姓名搜寻,建议至进阶搜寻限定作者字段,可获得较完整数据
  • 进阶搜寻
    主页登入上传说明关于NHRI管理 到手机版


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/2752


    题名: Expression of cytoplasmic-domain substituted epidermal growth factor receptor inhibits tumorigenicity of EGFR-overexpressed human glioblastoma multiforme
    作者: Liu, KJ;Chen, CT;Hu, WS;Hung, YM;Hsu, CY;Chuang, BF;Juang, SH
    贡献者: National Institute of Cancer Research
    摘要: The accumulated results of recent clinical studies have indicated that aberrant epidermal growth factor receptor (EGFR) activation due to gene amplification and/or rearrangement contributes to increased malignancy and poor prognosis in many human cancers, especially in human glioblastoma multiforme (GBM). The elevated EGFR signaling in GBM has been correlated with shorter interval to relapse and lower survival rates, even in patients treated with surgery, radiation therapy, and/or chemotherapy. Therefore, the blockade of EGFR signaling in GBM may provide an ideal alternative therapeutic strategy. In this study, two EGFR-overexpressing human GBM cell lines (i.e., DBTRG and GBM 8901) were used as a model system. We demonstrated that expression of a human EGFR (EGFR(t)-EGFP) chimera protein in which the cytoplasmic domain is substituted by EGFP significantly reduced the EGF-induced endogenous EGFR autophosphorylation, EGF-induced downstream extracellular signal-regulated kinase (ERK) and Akt signaling, and the proportion of internalized receptors in EGF stimulated cells. Furthermore, these cells' anchorage-independent growth in vitro was decreased and their tumorigenicity in vivo abrogated or strongly suppressed. Our data suggest that EGFR(t)-EGFP abrogates tumor growth by disrupting receptor activation via competing for EGF-like ligands, forming non-activated heterodimers with endogenous EGFR, and inhibiting the EGFR endosomal signaling by substantially diminishing receptor internalization. This treatment modality (termed 'dominant-negative EGFR therapy') and its efficacy for gliomas or other tumors are under scrutiny.
    关键词: Oncology
    日期: 2004-03
    關聯: International Journal of Oncology. 2004 Mar;24(3):581-590.
    Link to: http://www.ncbi.nlm.nih.gov/sites/entrez?myncbishare=nhrilib&Db=pubmed&Cmd=DetailsSearch&Term=14767543
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1019-6439&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000188956800014
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=6044226729
    显示于类别:[莊聲宏(1997-2004)] 期刊論文
    [劉柯俊] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    ISI000188956800014.pdf2100KbAdobe PDF822检视/开启


    在NHRI中所有的数据项都受到原著作权保护.

    TAIR相关文章

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