國家衛生研究院 NHRI:Item 3990099045/7018
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 12190/12972 (94%)
造訪人次 : 1060974      線上人數 : 720
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜尋範圍 查詢小技巧:
  • 您可在西文檢索詞彙前後加上"雙引號",以獲取較精準的檢索結果
  • 若欲以作者姓名搜尋,建議至進階搜尋限定作者欄位,可獲得較完整資料
  • 進階搜尋
    主頁登入上傳說明關於NHRI管理 到手機版
    請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/7018


    題名: Overexpression of Discoidin Domain Receptor 1 (DDR1) in oral squamous cell carcinoma
    作者: Tsai, WH;Chen, YL;Chen, HC;Cheng, AJ;Chang, KY;Chu, PY;Hsiao, JR;Chang, JY;Lin, SF
    貢獻者: National Institute of Cancer Research
    摘要: Overexpression and mutation of protein tyrosine kinases (PTKs) are observed in a variety of human cancers, which are associated with poor prognosis. To identify PTKs that are overexpressed in oral cancer, the expressions of eighty-three PTKs in four Taiwanese oral squamous cell carcinoma (OSCC) lines and a pooled cDNA reference were compared by quantitative RT-PCR analysis. Among several hits, we found DDR1 was consistently over-represented in a panel of OSCC cell lines. In addition, by immunohistochemistry analysis of clinical OSCC specimens, we observed that DDR1 concentrations were positively correlated with tumor grades. Similarly, results from microarray analysis of forty tumor/normal-paired oral cancer biopsies revealed an average ~1.5-fold elevation of DDR1 expressions in the tumor parts relative to the normal parts. DDR1 is a non-integrin collagen receptor that has been implicated in a variety of malignancies including breast, prostate, brain, and hepatocellular carcinomas. By using shRNA-mediated depletion of DDR1 in OSCC cells, we found that DDR1 signaling pathway, including phosphorylation of AKT, phosphorylation of ERK1/2 and Bcl-2 expression, plays a critical role in OSCC cell growth. Furthermore, results of immunoprecipitationwestern blot analysis showed that the overexpressed DDR1 was tyrosinephosphorylated and known ligands of DDR1 (collagens I and IV) did not further enhance its phosphorylation state, indicating that DDR1 in these OSCC cells is constitutively-active and is ligand-independent. Finally, imatinib mesylate (Glivec/ Gleevec), a potent DDR1 inhibitor, was found to inhibit the growth of OSCC cells in a dose- and time-dependent manner. This result reinforces the role of DDR1 in OSCC cell survival. Collectively, our data suggest that DDR1 could be a novel therapeutic target for oral cancer treatment.
    日期: 2012-11
    關聯: European Journal of Cancer. 2012 Nov;48(Suppl. 6):167.
    Link to: http://dx.doi.org/10.1016/S0959-8049(12)72340-7
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0959-8049&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000312763000535
    顯示於類別:[林素芳] 會議論文/會議摘要
    [張光裕] 會議論文/會議摘要
    [張俊彥] 會議論文/會議摘要

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    ISI000312763000535.pdf61KbAdobe PDF653檢視/開啟


    在NHRI中所有的資料項目都受到原著作權保護.

    TAIR相關文章

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