國家衛生研究院 NHRI:Item 3990099045/7428
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 855421      Online Users : 1096
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/7428


    Title: Enhanced cell growth and tumorigenicity of rat glioma cells by stable expression of human CD133 through multiple molecular actions
    Authors: Fang, KM;Lin, TC;Chan, TC;Ma, SZ;Tzou, BC;Chang, WR;Liu, JJ;Chiou, SH;Yang, CS;Tzeng, SF
    Contributors: Center for Nanomedicine Research
    Abstract: CD133 (Prominin-1/AC133) is generally treated as a cell surface marker found on multipotent stem cells and tumor stem-like cells, and its biological function remains debated. Genetically modified rat glioma cell lines were generated by lentiviral gene delivery of human CD133 into rat C6 glioma cells (hCD133(+)-C6) or by infection of C6 cells with control lentivirus (mock-C6). Stable hCD133 expression promoted the self-renewal ability of C6-formed spheres with an increase in the expression of the stemness markers, Bmi-1 and SOX2. Akt phosphorylation, Notch-1 activation, and Notch-1 target gene expression (Hes-1, Hey1 and Hey2) were increased in hCD133(+)-C6 when compared to mock-C6. (+)-C6 cells effectively suppressed their clonogenic ability, indicating that these factors are involved in expanding the growth of hCD133(+)-C6. An elevated expression of G (+)-C6. A decline in the invasion of hCD133(+)-C6 by knockdown of Arhgap27 expression indicated the critical role of Arhgap27 in promoting cell migration of hCD133(+)-C6. In vivo study further showed that hCD133(+)-C6 formed aggressive tumors in vivo compared to mock-C6. Exposure of hCD133(+)-C6 to arsenic trioxide not only reduced Akt phosphorylation, Notch-1 activation and Hes-1 expression in vitro, but also inhibited their tumorigenicity in vivo. (+)-C6 in vitro, as well as progressive tumor formation in vivo.
    Date: 2013-09
    Relation: Glia. 2013 Sep;61(9):1402-1417.
    Link to: http://dx.doi.org/10.1002/glia.22521
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0894-1491&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000322331700002
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84880771285
    Appears in Collections:[Chung-Shi Yang] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    ISI000322331700002.pdf1658KbAdobe PDF575View/Open


    All items in NHRI are protected by copyright, with all rights reserved.

    Related Items in TAIR

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