English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 45422/58598 (78%)
造訪人次 : 2514689      線上人數 : 146
RC Version 7.0 © 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


    請使用永久網址來引用或連結此文件: http://libir.tmu.edu.tw/handle/987654321/5284


    題名: 抗黴菌藥抑制人類惡性腫瘤細胞生長之分子機制
    Studies on the Molecular Mechanisms of Antifungal Agents-induced Human Malignant Cells Growth Arrest
    作者: 陳容甄
    Rong-Jane Chen
    貢獻者: 醫學研究所
    關鍵詞: 抗真菌劑
    細胞週期
    細胞凋亡
    p53 蛋白
    p21 蛋白
    細胞週期停滯
    antifungal agents
    cell cycle
    apoptosis
    p53 protein
    p21 protein
    cell cycle arrest
    日期: 2000
    上傳時間: 2009-09-11 15:29:10 (UTC+8)
    摘要: 中文摘要
    Ketoconazole與Terbinafine 是臨床上時常被使用的口服抗黴菌藥，且Ketoconazole已經被用於治療人體某些依賴荷爾蒙生長的癌症上。本研究證實Ketoconazole與Terbinafine能使癌細胞的生長週期停滯在G0/G1時期，進而抑制癌細胞的生長。藉由流式細胞儀的分析以及細胞生長曲線的分析，我們觀察到Ketoconazole與Terbinafine誘發癌細胞生長週期停滯的效果，在COLO 205 細胞 (具有wild-type p53) 比HT 29 (p53 His 273 突變) 和Hep 3B細胞 (缺少p53基因) 要好。由此我們推論p53的表現和 Ketoconazole與Terbinafine所引發的癌細胞G0/G1時期停滯的過程有某些相關性。我們藉由Ketoconazole或Terbinafine處理的COLO 205細胞中加入p53 antisense oligonucleotides 的實驗來證實這點推論。同時，Ketoconazole與Terbinafine會引起大腸癌細胞株p53，p21，p27等蛋白質表現量增加，且相對的抑制Cyclin D3及CDK4等蛋白質的表現，且Terbinafine誘發HL 60細胞凋亡的發生。在裸鼠的實驗上也證實Ketoconazole及Terbinafine抑制COLO 205腫瘤生長。本研究提出Ketoconazole與Terbinafine誘發大腸癌細胞生長週期停滯的分子機制，也因為Ketoconazole與Terbinafine具備這些效果，我們認為Ketoconazole與Terbinafine可成為具有潛力的癌症治療藥物。
    Abstract
    In this study, we demonstrated that Ketoconazole (KT) and Terbinafine (TB), two widely used oral-antifungal agents inhibit cell cycle progression in human colorectal and hepatic cancer cell lines in G0/G1 phase. Human cancer cells with various p53 statuses were used to investigate the mechanisms of KT- and TB-induced G0/G1 arrest. The results of flow cytometry and cell growth curve analyses revealed that KT and TB-induced growth arrest was more profound in COLO 205 (with wild-type p53) than in HT 29 (p53 His273 mutant) and Hep 3B (with deleted p53). By the way, TB induced apoptosis in HL 60 cells. KT and TB increased the expression of p53, p21, and p27 in cancer cells, and inhibited the expression of CyclinD3 and CDK4 proteins leaded to the growth arrest in human cancer cells. In contrast, the expression of PCNA, as well as cyclin A, D1, and E levels in human cancer cells were not significant change as compared with untreated cells. CDK4 and CDK2 kinase activity from cells treated with KT and TB was markedly inhibited. In nude mice experiments, treated with KT or TB inhibit the growth of human COLO 205 tumor. Taken together, these results suggest universality of KT and TB in cessation of cell proliferation, also make them very attractive agents for use as potential cancer chemotherapeutic agents.
    資料類型: thesis
    顯示於類別:[醫學科學研究所] 博碩士論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    摘要.doc32KbMicrosoft Word100檢視/開啟
    摘要.pdf61KbAdobe PDF123檢視/開啟
    摘要.ppt143KbMicrosoft Powerpoint110檢視/開啟
    摘要.ps324KbPostscript55檢視/開啟


    在TMUIR中所有的資料項目都受到原著作權保護.

    TAIR相關文章

    著作權聲明 Copyright Notice

    • 本平台之數位內容為臺北醫學大學所收錄之機構典藏，包含體系內各式學術著作及學術產出。秉持開放取用的精神，提供使用者進行資料檢索、下載與取用，惟仍請適度、合理地於合法範圍內使用本平台之內容，以尊重著作權人之權益。商業上之利用，請先取得著作權人之授權。

      The digital content on this platform is part of the Taipei Medical University Institutional Repository, featuring various academic works and outputs from the institution. It offers free access to academic research and public education for non-commercial use. Please use the content appropriately and within legal boundaries to respect copyright owners' rights. For commercial use, please obtain prior authorization from the copyright owner.

    • 瀏覽或使用本平台，視同使用者已完全接受並瞭解聲明中所有規範、中華民國相關法規、一切國際網路規定及使用慣例，並不得為任何不法目的使用TMUIR。

      By utilising the platform, users are deemed to have fully accepted and understood all the regulations set out in the statement, relevant laws of the Republic of China, all international internet regulations, and usage conventions. Furthermore, users must not use TMUIR for any illegal purposes.

    • 本平台盡力防止侵害著作權人之權益。若發現本平台之數位內容有侵害著作權人權益情事者，煩請權利人通知本平台維護人員([email protected])，將立即採取移除該數位著作等補救措施。

      TMUIR is made to protect the interests of copyright owners. If you believe that any material on the website infringes copyright, please contact our staff([email protected]). We will remove the work from the repository.

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