ASIA unversity:Item 310904400/112424
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 90453/105671 (86%)
造访人次 : 16042580      在线人数 : 85
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/310904400/112424


    题名: Thrombospondin enhances RANKL-dependent osteoclastogenesis and facilitates lung cancer bone metastasis
    作者: Wang, Maofeng;Wang, Maofeng;Ch, Chia-Chia;Chao, Chia-Chia;陳?均;Liu, Po-I.;Liu, Po-I.;Yang, Yi-Chen;Yang, Yi-Chen;Su, Chen-Ming;Su, Chen-Ming;黃偉謙;Huang, Wei-Chien;湯智昕;Chih-Hsin;Tang
    贡献者: 生物科技學系
    日期: 2019-05
    上传时间: 2019-11-08 11:49:27 (UTC+8)
    摘要: Lung cancers have a predilection for metastasizing to bone. The matricellular glycoprotein thrombospondin (TSP)-2 regulates multiple biological functions and has a critical role in tumor development and metastasis, although its effects are uncertain in lung cancer bone metastasis. This study demonstrates that TSP-2 expression is highly correlated with lung cancer tumor stage and that the TSP-2 neutralizing antibody reduces osteoclast formation in conditioned medium obtained from lung cancer cells. We also found that TSP-2 promotes osteoclastogenesis through the RANKL-dependent pathway and that TSP-2-mediated osteoclastogenesis involves the transactivation of nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) via the inhibition of miR-486-3p expression. Osteoblasts played a critical role in osteoclast differentiation and incubation of osteoblasts with TSP-2 altered the RANKL:OPG ratio. Furthermore, TSP-2 knockdown inhibited lung cancer osteolytic metastasis in vivo. TSP-2 appears to be worth targeting for the prevention of bone metastasis in lung cancer.
    關聯: BIOCHEMICAL PHARMACOLOGY
    显示于类别:[生物科技學系] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    index.html0KbHTML191检视/开启


    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