中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/46179
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 29490/55136 (53%)
造访人次 : 1517716      在线人数 : 407
RC Version 7.0 © 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CMUR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.cmu.edu.tw/ir/handle/310903500/46179


    题名: 介白素-6在人類骨肉瘤細胞的移行中扮演之角色
    The role of IL-6 in the cell motility of human osteosarcoma cells
    作者: 張子玲;Chang, Zi-Ling
    贡献者: 基礎醫學研究所碩士班
    关键词: 介白素-6;骨肉瘤;細胞間黏附因子;細胞移行;Interleukin-6;Osteosarcoma;ICAM-1;Cell motility
    日期: 2012-01-19
    上传时间: 2012-08-31 16:33:57 (UTC+8)
    出版者: 中國醫藥大學
    摘要: 骨肉瘤是最常見的原發性骨腫瘤,多數好發於童年和青春期,其特點為高度惡性和轉移潛能。此外有文獻證實許多癌細胞皆會有高表現量的介白素-6 (Interleukin-6; IL-6)。IL-6為具有多重免疫調節功能的細胞激素,屬於一種分泌型的細胞激素,會和IL-6R (Interleukin 6 receptor) 結合進而調控人類癌症細胞的增生、細胞凋亡、轉移及侵襲等。然而IL-6對於人類骨肉瘤移動性的機制目前不是很清楚。我們發現IL-6會促進人類骨肉瘤細胞移行能力和增加細胞間黏附因子 (Intercellular adhesion molecule-1; ICAM-1) 的表現。前處理IL-6中和性抗體、ILK抑制劑 (Kp392) 和Akt的抑制劑 (Akti) 會抑制IL-6增加人類骨肉瘤細胞移行的能力和ICAM-1的表現。在IL-6的刺激下會增加ILK及Akt磷酸化。除此之外,c-Jun抑制劑也會降低IL-6增加細胞移行能力和ICAM-1的表現。另外,IL-6也會促進c-Jun入核並結合到ICAM-1啟動子上之AP-1 element。綜合以上結果,IL-6促進ICAM-1表現經由與IL-6R的結合及ILK及Akt的訊息傳導進而活化c-Jun, 而造成人類骨肉瘤細胞株的移動性。
    Osteosarcoma is the most common primary bone tumor associated with childhood and adolescence. It is characterized by high malignant and metastatic potential. Recently, some studies found that interleukin-6 (IL-6) is highly expressed in many cancer cells. However, the effects of IL-6 on cell motility and intercellular adhesion molecule-1 (ICAM-1) expression in human osteosarcoma cells are rarely known. Here we found that IL-6 induced the cell motility and expression of ICAM-1 in human osteosarcoma cells. IL-6R monoclonal antibody (mAb), integrin-linked kinase inhibitor (Kp392) and Akt inhibitor inhibited IL-6-induced cell mobility and ICAM-1 expression. IL-6 stimulation increased the phosphorylation of ILK and Akt. In addition, c-Jun inhibitor (curcumin and tanshinone-IIA) also antagonized IL-6 increased cell motility and ICAM-1 expression. Moreover, IL-6 induced the binding of c-Jun to the AP-1 element on the ICAM-1 promoter. Taken together, our results suggested that IL-6 enhances motility of osteosarcoma cells by increasing ICAM-1 expression through the IL-6R, ILK, Akt, and AP-1 signal transduction pathway.
    显示于类别:[基礎醫學研究所] 博碩士論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    index.html0KbHTML45检视/开启


    在CMUR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