ASIA unversity:Item 310904400/81134
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 94286/110023 (86%)
造訪人次 : 21666771      線上人數 : 1056
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


    請使用永久網址來引用或連結此文件: http://asiair.asia.edu.tw/ir/handle/310904400/81134


    題名: Suppression of Dicer Increases Sensitivity to Gefitinib in Human Lung Cancer Cells
    作者: Jui-Chieh Chen;Yen-Hao Su;Yang-Hao Yu;Yi-Wen Chang;Ching-Feng Chiu;Chi-Feng Tseng;Hsin-An Chen;Jen-Liang Su
    貢獻者: 生物科技學系
    日期: 2014-04
    上傳時間: 2014-10-01 08:32:40 (UTC+0)
    摘要: Background
    Accumulating evidence is revealing an important role of microRNA (miRNA) in tumor progression and chemotherapeutic resistance. Dicer is a cytoplasmic endoribonuclease type III crucial for production of mature miRNAs. The aberrant expression of Dicer has also been reportedly associated with clinical aggressiveness, prognosis, and patient survival in various cancer types. However, the molecular mechanisms of Dicer in acquired gefitinib resistance are still not clear.
    Methods
    In this study, we analyzed the protein level of Dicer between gefitinib-sensitive (PC9) and gefitinib-resistant (PC9/GR) non-small-cell lung cancer (NSCLC) cell lines by Western blot analysis. Silence and overexpression of the Dicer were performed to investigate the effects on gefitinib sensitivity, as assessed by (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay and sub-G1 assay of flow cytometry. To further explore the mechanism of chemoresistance, we examined whether Dicer knockdown led to modulating specific miRNAs and its miRNA target genes.
    Results
    Dicer expression was significantly increased in PC9/GR compared with PC9 cells. Knockdown of Dicer restores gefitinib sensitivity in resistant cells, and overexpression of Dicer enhances resistance to gefitinib in sensitive cells. Silencing of Dicer induces sensitivity to gefitinib in NSCLC cells through the downregulation of miR-30b/c and miR-221/222 to increase the protein level of caspase-3, resulting in an increase in gefitinib-induced apoptosis.
    Conclusions
    Dicer contributes to the resistance to gefitinib in lung cancer. These results indicate that Dicer may be a target for diagnosis and therapy of patients with resistance to gefitinib.
    關聯: ANNALS OF SURGICAL ONCOLOGY,21(4),555-563.
    顯示於類別:[生物科技學系] 期刊論文

    文件中的檔案:

    檔案 大小格式瀏覽次數
    index.html0KbHTML431檢視/開啟


    在ASIAIR中所有的資料項目都受到原著作權保護.

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