ASIA unversity:Item 310904400/111348
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 90453/105671 (86%)
造访人次 : 16036781      在线人数 : 117
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


    题名: Differential Characterization of Temozolomide-Resistant Human Glioma Cells.
    作者: La, Sheng-Wei;Lai, Sheng-Wei;Huan, Bor-Ren;Huang, Bor-Ren;Liu, Yu-Shu;Liu, Yu-Shu;Li, Hsiao-Yun;Lin, Hsiao-Yun;Chun-Chuan, Chun-Chuan C;Chen, Chun-Chuan;蔡政芳;Tsai, Cheng-Fang;盧大宇;Lu, Dah-Yuu;*;Lin, Chingju;Lin, Chingju
    贡献者: 生物科技學系
    日期: 2018-01
    上传时间: 2018-08-20 09:44:00 (UTC+8)
    摘要: Glioblastoma multiforme (GBM) is the most common type of primary and malignant tumor occurring in the adult central nervous system. Temozolomide (TMZ) has been considered to be one of the most effective chemotherapeutic agents to prolong the survival of patients with glioblastoma. Many glioma cells develop drug-resistance against TMZ that is mediated by increasing O-6-methylguanine-DNA methyltransferase (MGMT) levels. The expression of connexin 43 was increased in the resistant U251 subline compared with the parental U251 cells. The expression of epithelial–mesenchymal transition (EMT)-associated regulators, including vimentin, N-cadherin, and β-catenin, was reduced in the resistant U251 subline. In addition, the resistant U251 subline exhibited decreased cell migratory activity and monocyte adhesion ability compared to the parental U251 cells. Furthermore, the resistant U251 subline also expressed lower levels of vascular cell adhesion molecule (VCAM)-1 after treatment with recombinant tumor necrosis factor (TNF)-α. These findings suggest differential characteristics in the drug-resistant GBM from the parental glioma cells.

    Keywords: glioblastoma, temozolomide, connexin 43, drug-resistant
    显示于类别:[生物科技學系] 期刊論文


    档案 大小格式浏览次数


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