國家衛生研究院 NHRI:Item 3990099045/3064
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 12145/12927 (94%)
造訪人次 : 861836      線上人數 : 806
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜尋範圍 查詢小技巧：
  • 您可在西文檢索詞彙前後加上"雙引號"，以獲取較精準的檢索結果
  • 若欲以作者姓名搜尋，建議至進階搜尋限定作者欄位，可獲得較完整資料
    •  進階搜尋
    主頁 ‧ 登入 ‧ 上傳 ‧ 說明 ‧ 關於NHRI ‧ 管理 到手機版
    國家衛生研究院 NHRI > 癌症研究所 > 其他 > 期刊論文 >  Item 3990099045/3064


    請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/3064


    題名: SFRP1 suppressed hepatoma cells growth through Wnt canonical signaling pathway
    作者: Shih, YL;Hsieh, CB;Lai, HC;Yan, MD;Hsieh, TY;Chao, YC;Lin, YW
    貢獻者: National Institute of Cancer Research
    摘要: Oncogenic activation of the Wnt/beta-catenin signaling pathway is common in hepatocellular carcinoma (HCC). The secreted frizzled-related proteins (SFRPs) function as negative regulators of Writ signaling and have important implications for carcinogenesis. Promoter hypermethylation of SFRP genes is common in human cancers. However, the role of SFRPs in HCC is not clear. Recently, we have shown that SFRP1 is frequently downregulated through promoter hypermethylation. To confirm and extend these findings, the methylation status of the other SFRP members, including SFRP2, SFRP4 and SFRP5, was examined by methylation-specific polymerase chain reaction (MS-PCR). Hypermethylation of SFRP genes, except for SFRP4, is frequent in HCCs and the levels found here were significantly higher than those seen in cirrhotic livers, chronic hepatitis livers and normal controls (P < 0. 0001 for SFRP1 and SFRP2, p < 0.05 for SFRP5). To investigate the role of SFRP1 in HCCs, we used re-expression of SFRP1 in Pcatenin-dependent HCC cell lines: Huh6 and HepG2. Restoration of SFRP1 attenuated Writ signaling in those Huh6 hepatoma cells with a beta-catenin gene point mutation, decreased abnormal accumulation of beta-catenin in the nucleus and suppressed cell growth. Conversely, restoration of SFRP1 in HepG2 hepatoma cells with truncated beta catenin could not block the Writ signaling pathway. Furthermore, knocking down SFRP1 by RNA interference in beta-catenin-deficient cell lines (SK-Hep1) stimulated Wnt signaling and promoted cell growth. Our data suggested that SFRP1 suppressed liver cancer cells growth through Wnt canonical signaling. Moreover, beta-cateninindependent noncanonical pathway might be involved in Wnt signaling activation through unknown molecules in HCC.
    關鍵詞: Oncology
    日期: 2007-09-01
    關聯: International Journal of Cancer. 2007 Sep;121(5):1028-1035.
    Link to: http://dx.doi.org/10.1002/ijc.22750
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0020-7136&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000248242500013
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34547093863
    顯示於類別:[其他] 期刊論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    000248242500013.pdf445KbAdobe PDF708檢視/開啟


    在NHRI中所有的資料項目都受到原著作權保護.

    TAIR相關文章

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