國家衛生研究院 NHRI:Item 3990099045/2775
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 12145/12927 (94%)
造訪人次 : 912591      線上人數 : 1224
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


    請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/2775


    題名: Involvement of nuclear transcription factor-kappa B in low-dose doxorubicin-induced drug resistance of cervical carcinoma cells
    其他題名: Involvement of nuclear transcription factor-κB in low-dose doxorubicin-induced drug resistance of cervical carcinoma cells
    作者: Yeh, PY;Chuang, SE;Yeh, KH;Song, YC;Cheng, AL
    貢獻者: National Institute of Cancer Research
    摘要: Administration of suboptimal doses of anticancer drugs not only fails to control tumor but often results in increased drug resistance of tumor cells. However, little is known about the effects of transient exposure to a minimally cytotoxic dose of chemotherapy on the development of drug resistance of the tumors. Previous studies have shown that upregulation of drug-exporter proteins (ATP-binding-cassette proteins) may be one of the key mechanisms involved in inducible drug resistance. In this study, we demonstrated that upregulation of NF-KB is another possible mechanism. SiHa cells were exposed to low-dose doxorubicin (100 nM; IC30) for 3 hr, and then were continuously cultured in drug-free culture media (designated as SiHa/DR cells). SiHa/DR cells at up to 9 passages showed increased resistance to doxorubicin and cross-resistance to cisplatin. Results of quantitative real-time PCR and flow cytometry assay indicated that the increased drug-resistance in SiHa/DR cells was not due to upregulation of drug-exporter proteins or to the decrease of intracellular concentration of anticancer drugs. Both the basal and drug-induced NF-KB activity were shown to be increased in SiHa/DR cells by EMSA and NF-KB-driven luciferase reporter gene assay. Suppression of NF-KB activation by transfection of a dominant negative IKBalpha prevented the development of drug resistance, indicating that the upregulated NF-KB activity was positively correlated with the low-dose doxorubicin-induced drug resistance. These results suggest that even a transient exposure to a small dose of anticancer drugs may induce drug resistance in some cancer cells via upregulation of NF-KB activity. (C) 2003 Elsevier Science Inc. All rights reserved.
    關鍵詞: Pharmacology & Pharmacy
    日期: 2003-07-01
    關聯: Biochemical Pharmacology. 2003 Jul;66(1):25-33.
    Link to: http://dx.doi.org/10.1016/S0006-2952(03)00250-8
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0006-2952&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000183820100003
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0038682199
    顯示於類別:[莊雙恩] 會議論文/會議摘要

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    000183820100003.pdf509KbAdobe PDF998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