ASIA unversity:Item 310904400/86944
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 90120/105278 (86%)
造访人次 : 8950257      在线人数 : 65
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/310904400/86944


    题名: Vascular Endothelial Growth Factor-C Upregulates Cortactin and Promotes Metastasis of Esophageal Squamous Cell Carcinoma
    作者: Chih-Ming Su;Yen-Hao Su;Ching-Feng Chiu;Yi-Wen Chang;Chih-Chen Hong;Yang-Hao Yu;Yuan-Soon Ho;Chih-Hsiung Wu;Chia-Sheng Yen;Jen-Liang Su
    贡献者: 生物科技學系
    日期: 2014-09
    上传时间: 2014-11-07 14:54:56 (UTC+8)
    摘要: Background
    Vascular endothelial growth factor-C (VEGF-C) plays an important role during cancer progression and metastasis through activation of VEGF receptors. However, the role of VEGF-C in esophageal squamous cell carcinoma (ESCC) remains unclear.
    Methods
    The expression of VEGF-C in advanced stages of esophageal cancer was examined by immunohistochemistry and its expression was correlated with the protein level of cortactin (CTTN) by Western blot. Knockdown and overexpression of the CTTN protein were respectively performed to investigate the effects on VEGF-C-enhanced ESCC migration/invasion by in vitro transwell assay, cell tracing assay, and tumor growth/experimental metastasis in animal models.
    Results
    The expression of VEGF-C was positively correlated with tumor status and poor clinical prognosis in patient with esophageal cancer. VEGF-C-upregulated CTTN expression contributed the migration/invasive abilities of ESCC cell lines through Src-mediated downregulation of miR-326. Moreover, knockdown of CTTN expression significantly abolished VEGF-C-induced tumor growth and experimental lung metastasis in vivo.
    Conclusions
    Upregulation of CTTN is critical for VEGF-C-mediated tumor growth and metastasis of ESCC. These finding suggest that VEGF-C upregulated CTTN expression through Src-mediated downregulation of miR-326. CTTN may be a crucial mediator of VEGF-C-involved ESCC metastasis, which provides a potential target for diagnosis and individualized treatment in clinical practice.
    關聯: ANNALS OF SURGICAL ONCOLOGY,21(Suppl 4):S767-775.
    显示于类别:[生物科技學系] 期刊論文

    文件中的档案:

    没有与此文件相关的档案.



    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