National Changhua University of Education Institutional Repository : Item 987654321/17887
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 6491/11663
造访人次 : 24894914      在线人数 : 66
RC Version 3.2 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 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://ir.ncue.edu.tw/ir/handle/987654321/17887

题名: Glial Cell-derived Neurotrophic Factor Increases Migration of Human Chondrosarcoma Cells Via ERK and NF-κB Pathways
作者: Su, Chen-Ming;Yang, Shu-Ning;Tang, Chih-Hsin;Tseng, Wen-Pei
贡献者: 運動健康所
日期: 2009-04
上传时间: 2014-01-15T04:04:16Z
出版者: American Association for Cancer Research
摘要: Invasion of tumor cells is the primary cause of therapeutic failure in the treatment of malignant chondrosarcomas. Glial cell-derived neurotrophic factor (GDNF) plays a crucial role in migration and metastasis of human cancer cells. Integrins are the major adhesive molecules in mammalian cells. Here we found that GDNF directed the migration and increased cell surface expression of alphav and beta3 integrin in human chondrosarcoma cells. Pretreated of JJ012 cells with MAPK kinase (MEK) inhibitors PD98059 or U0126 inhibited the GDNF-mediated migration and integrin expression. Stimulation of cells with GDNF increased the phosphorylation of MEK and extracellular signal-regulating kinase (ERK). In addition, NF-kappaB inhibitor (PDTC) or IkappaB protease inhibitor (TPCK) also inhibited GDNF-mediated cells migration and integrin up-regulation. Stimulation of cells with GDNF induced IkappaB kinase (IKKalpha/beta) phosphorylation, IkappaB phosphorylation, p65 Ser(536) phosphorylation, and kappaB-luciferase activity. Furthermore, the GDNF-mediated increasing of kappaB-luciferase activity was inhibited by PD98059, U0126, PDTC and TPCK or MEK, ERK, IKKalpha, and IKKbeta mutants. Taken together, these results suggest that the GDNF acts through MEK/ERK, which in turn activates IKKalpha/beta and NF-kappaB, resulting in the activations of alphavbeta3 integrin and contributing the migration of human chondrosarcoma cells.
關聯: The 100th American Association for Cancer Research (AACR)Annual Meeting
显示于类别:[運動健康研究所] 會議論文

文件中的档案:

档案 大小格式浏览次数
2070200316002.pdf51KbAdobe PDF433检视/开启


在NCUEIR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