ASIA unversity:Item 310904400/16660
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 90429/105609 (86%)
造访人次 : 10534188      在线人数 : 486
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


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://asiair.asia.edu.tw/ir/handle/310904400/16660


    题名: Nuclear Translocation of Epidermal Growth Factor Receptor by Akt-dependent Phosphorylation Enhances Breast Cancer-resistant Protein Expression in Gefitinib-resistant Cells
    作者: 黃偉謙;Huang, Wei-Chien;李龍緣;Li, Long-Yuan;Chang, Wei-Chao;Chang, Wen-Chang;Chen, Andy Jer-En;Tsai, Chang-Hai
    贡献者: 生物科技學系
    关键词: Drug Resistance;Gene Regulation, Nuclear Translocation;Protein Phosphorylation;Receptor-tyrosine Kinase;Akt;BCRP/ABCG2;Gefitinib, Nuclear EGFR
    日期: 2011-06
    上传时间: 2012-11-23 17:15:35 (UTC+8)
    摘要: Epidermal growth factor receptor (EGFR), an aberrantly overexpressed or activated receptor-tyrosine kinase in many cancers, plays a pivotal role in cancer progression and has been an attractive target for cancer therapy. Gefitinib and erlotinib, two EGFR-tyrosine kinase inhibitors, have been approved for non-small cell lung cancer. However, durable clinical efficacy of these EGFR inhibitors is severely limited by the emergence of acquired resistance. For example, the expression of breast cancer-resistant protein (BCRP/ABCG2) has been shown to confer acquired resistance of wild-type EGFR (wtEGFR)-expressing cancer cells to gefitinib. However, the underlying molecular mechanisms still remain unclear. Here, we show that wtEGFR expression is elevated in the nucleus of acquired gefitinib-resistant cancer cells. Moreover, nuclear translocation of EGFR requires phosphorylation at Ser-229 by Akt. In the nucleus, EGFR then targets the proximal promoter of BCRP/ABCG2 and thereby enhances its gene transcription. The nuclear EGFR-mediated BCRP/ABCG2 expression may contribute at least in part to the acquired resistance of wtEGFR-expressing cancer cells to gefitinib. Our findings shed light on the role of nuclear EGFR in the sensitivity of wtEGFR-expressing cancer cells to EGFR tyrosine kinase inhibitors and also deciphered a putative molecular mechanism contributing to gefitinib resistance through BCRP/ABCG2 expression.
    關聯: JOURNAL OF BIOLOGICAL CHEMISTRY
    显示于类别:[生物科技學系] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    index.html0KbHTML129检视/开启


    在ASIAIR中所有的数据项都受到原著作权保护.


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