國家衛生研究院 NHRI:Item 3990099045/15381
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12145/12927 (94%)
造访人次 : 907173      在线人数 : 855
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/3990099045/15381


    题名: Intervention of AXL in EGFR signaling via phosphorylation and stabilization of MIG6 in non-small cell Lung cancer
    作者: Yang, YY;Lin, SC;Lay, JD;Cho, CY;Jang, T;Ku, HY;Yao, CJ;Chuang, SE
    贡献者: National Institute of Cancer Research
    摘要: About 80% of lung cancer patients are diagnosed with non-small cell lung cancer (NSCLC). EGFR mutation and overexpression are common in NSCLC, thus making EGFR signaling a key target for therapy. While EGFR kinase inhibitors (EGFR-TKIs) are widely used and efficacious in treatment, increases in resistance and tumor recurrence with alternative survival pathway activation, such as that of AXL and MET, occur frequently. AXL is one of the EMT (epithelial-mesenchymal transition) signature genes, and EMT morphological changes are also responsible for EGFR-TKI resistance. MIG6 is a negative regulator of ERBB signaling and has been reported to be positively correlated with EGFR-TKI resistance, and downregulation of MIG6 by miR-200 enhances EMT transition. While MIG6 and AXL are both correlated with EMT and EGFR signaling pathways, how AXL, MIG6 and EGFR interplay in lung cancer remains elusive. Correlations between AXL and MIG6 expression were analyzed using Oncomine or the CCLE. A luciferase reporter assay was used for determining MIG6 promoter activity. Ectopic overexpression, RNA interference, Western blot analysis, qRT-PCR, a proximity ligation assay and a coimmunoprecipitation assay were performed to analyze the effects of certain gene expressions on protein-protein interaction and to explore the underlying mechanisms. An in vitro kinase assay and LC-MS/MS were utilized to determine the phosphorylation sites of AXL. In this study, we demonstrate that MIG6 is a novel substrate of AXL and is stabilized upon phosphorylation at Y310 and Y394/395 by AXL. This study reveals a connection between MIG6 and AXL in lung cancer. AXL phosphorylates and stabilizes MIG6 protein, and in this way EGFR signaling may be modulated. This study may provide new insights into the EGFR regulatory network and may help to advance cancer treatment.
    日期: 2023-10-04
    關聯: International Journal of Molecular Sciences. 2023 Oct 04;24(19):Article number 14879.
    Link to: http://dx.doi.org/10.3390/ijms241914879
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1661-6596&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:001083230100001
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85174727070
    显示于类别:[莊雙恩] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    ISI001083230100001.pdf6024KbAdobe PDF90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