English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 45422/58598 (78%)
造訪人次 : 2534360      線上人數 : 199
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/987654321/57925


    題名: BEND5基因於大腸直腸癌之分子變異及臨床相關性研究
    Molecular Alteration Analysis of BEND5 Gene and Its Clinical Significance in Colorectal cancer
    作者: 黃雨芳
    Huang, Yu-Fang
    貢獻者: 林若凱
    關鍵詞: 大腸直腸癌;表顯遺傳;抑癌基因
    Colorectal cancer;epigenetic;tumor suppressor gene;Illumina human methylation 450K;tumor suppressor gene
    日期: 2014-06-26
    上傳時間: 2019-09-02 12:29:53 (UTC+8)
    摘要: 近年來，隨著環境及飲食習慣的改變，根據行政院衛生福利部國民健康局公布2011年台灣地區診斷為直腸結腸癌的個案有14040位，已躍為十大癌症發生率的第一名。儘管醫療的進步，直腸結腸癌的分子機轉仍尚未完全釐清。至今直腸結腸癌形成的原因是因為基因(genetic)和表顯遺傳(epigenetic) 修飾的改變所造成。而本研究目的找出大腸直腸癌具過度甲基化之基因BEND5，並深入探討BEND5 mRNA及啟 子甲基化之情形，於癌細胞中扮演的功能與角色之影響的致癌機轉，以助於了解BEND5於癌症變異情形及形成原因。
    　　本研究將從醫院取得的大腸直腸癌手術後臨床檢體，抽取DNA後做bisulfite convert DNA進行甲基化分析，利用Illumina Human Methylation450觀察到BEND5 promoter上有高度甲基化的情形;進一步以Real-time methylation specific PCR (qMSP) 偵測發現有82.35% (70/85位) BEND5 promoter上具高度甲基化的情形，特別是在有局部淋巴結轉移的病人癌組織中95.2% (20/21) (p= 0.030)。再利用Real-time PCR分析，相較於正常組織71% (24/34位) 病人的病灶BEND5 mRNA都是低表達。為了瞭解BEND5在癌細胞中所具有的功能，藉由大腸癌細胞株實驗將BEND5大量表現於大腸癌細胞中，可以看到細胞增殖的數目相對的比控制組少。若同時將大量表現BEND5的細胞剔除 BEND5 mRNA於細胞中的表現，其細胞增殖的數目回復到正常狀態。本研究推測BEND5在大腸癌形成可能扮演抑癌基因的角色。
    Colorectal cancer (CRC) is the most frequently diagnosed cancer in Taiwan. Colorectal cancer occurrence rates have been increasing in recent years. It was the third leading cause of cancer death on 2011. DNA methylation is common abnormality in colorectal cancer (CRC). Aberrant promoter hypermethylation of TSG-associated CpG islands can lead to transcriptional silencing and result in tumorigenesis. DNA methylation is catalyzed by enzymes known as DNA methyltransferases. We applied Illumina human methylation 450K to identify loci hypermethylation in 26 primary CRCs relative to non-neoplastic colorectal tissue. A candidate tumor suppressor gene, BEND5 showed 82.35% (70 of 85) hypermethylation in colorectal tumors compared to matched normal colorectal tissues, especially in patients with metastasis in regional lymph nodes 95.2% (20/21) (p = 0.030). This CRC-associated hypermathylation events were evaluated by quantitative methylation specific real-time PCR (qMSP-PCR). Using real-time PCR found 71% (24 of 34) BEND5 mRNA expression was down-regulation in CRCs compared to matched normal colorectal tissues. Transient transfection of BEND5 and/or si-BEND5 found BEND5 could inhibit colon cancer cell proliferation. In addition, BEND5 was expressed in nucleus by detecting immunofluorescence when BEND5 was transfected into cell line. In conclusion, BEND5 alteration may play an important role in colorectal cancer. The predominana mechanisms of BEND5 inactivation were BEND5 promoter hypermathylation. The present study suggested that the alteration of BEND5 may be involved in tumor development. We thought BEND5 is a candidate tumor suppressor gene in colorectal cance.
    描述: 碩士
    指導教授- 林若凱
    委員-蔡世峯
    委員-張偉嶠
    資料類型: thesis
    顯示於類別:[生藥學研究所] 博碩士論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    index.html0KbHTML268檢視/開啟


    檢視Licence

    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