國家衛生研究院 NHRI:Item 3990099045/3364
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    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/3364


    题名: Carbonic anhydrase III promotes transformation and invasion capability in hepatoma cells through FAK signaling pathway
    作者: Dai, HY;Hong, CC;Liang, SC;Yan, MD;Lai, GM;Cheng, AL;Chuang, SE
    贡献者: National Institute of Cancer Research
    摘要: Carbonic anhydrase III (CAIII) is distinguished from the other members of the CA family by low carbon dioxide hydratase activity, resistance to the CA inhibitor acetazolamide, and a predominant expression in the liver of males. In this report the effects of CAIII expression on liver cancer cells invasiveness were explored. Overexpression of CAIII in the HCC cell line SK-Hep1 resulted in increased anchorage-independent growth and invasiveness. And siRNA-mediated silencing of CAIII expression decreased the invasive ability of SK-Hep1 cells. Furthermore, CAIII transfectants showed elevated focal adhesion kinase (FAK) and Src activity. Silencing of FAK expression in CAIII transfectants led to suppression of HCC cell invasion. More importantly, the CAIII transfectants acidified the culture medium at an accelerated speed than the control cells did. Taken together, these data suggest that the CAIII-promoted invasive ability of HCC cells may probably be mediated through, at least in part, the FAK signaling pathway via intracellular and/or extracellular acidification. 穢 2008 Wiley-Liss, Inc.
    日期: 2008-12
    關聯: Molecular Carcinogenesis. 2008 Dec;47(12):956-963.
    Link to: http://dx.doi.org/10.1002/mc.20448
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0899-1987&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000261421000006
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=56749091610
    显示于类别:[莊雙恩] 期刊論文
    [賴基銘(2004-2008)] 期刊論文

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