Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/32686
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 18272/20499 (89%)
Visitors : 16043843      Online Users : 1415
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    請使用永久網址來引用或連結此文件: https://ir.cnu.edu.tw/handle/310902800/32686


    題名: Akt inhibitor SC66 promotes cell sensitivity to cisplatin in chemoresistant ovarian cancer cells through inhibition of COL11A1 expression
    作者: Wu, Yi-Hui
    Huang, Yu-Fang
    Chien-Chin Chen(陳建欽)
    Chou, Cheng-Yang
    貢獻者: Natl Cheng Kung Univ, Coll Med, Natl Cheng Kung Univ Hosp, Dept Obstet & Gynecol
    Chia Yi Christian Hosp, Depardnent Pathol
    Chia Nan Univ Pharm & Sci, Dept Cosmet Sci
    關鍵詞: PLECKSTRIN HOMOLOGY DOMAIN
    PROGNOSTIC-SIGNIFICANCE
    PI3K/AKT PATHWAY
    ACTIVATION
    BREAST
    GENE
    PIK3CA
    TWIST
    PROTEIN
    IDENTIFICATION
    日期: 2019-04
    上傳時間: 2020-07-29 13:55:16 (UTC+8)
    出版者: NATURE PUBLISHING GROUP
    摘要: We studied Akt inhibition using SC66 in a NOD-SCID xenograft mouse model and a panel of eight ovarian cancer cell lines. Elevated phospho-Akt levels in cancerous tissue were associated with short progression-free survival and overall survival. Cell sensitivity to SC66 was inversely correlated with phospho-Akt and COL11A1 expression levels, as well as resistance to cisplatin or paclitaxel. SC66 inhibited phosphorylation of Akt and its downstream effectors 4EBP1 and p70S6 kinase. SC66 also attenuated expression of TWIST1 and Mcl-1, factors important in cell invasiveness and antiapoptosis, respectively. SC66-sensitized chemoresistant cells to cisplatin and paclitaxel treatment, and promoted apoptosis. In addition, SC66 inhibited COL11A1 expression via decreased binding of CCAAT/enhancer-binding protein beta (c/EBP beta), reducing chemoresistance and decreasing binding of nuclear transcription factor Y (NF-YA) to COL11A1. A mouse xenograft experiment demonstrated that SC66 treatment caused a reduction in tumor formation and enhanced the therapeutic efficacy of cisplatin. This study demonstrates the role of Akt in ovarian tumor progression and chemoresistance, and supports the application of SC66 as a therapy for ovarian cancer.
    關聯: Cell Death & Disease, v.10, 322
    顯示於類別:[Dept. of Cosmetic Science and institute of cosmetic science] Periodical Articles

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    10.1038-s41419-019-1555-8.pdf2652KbAdobe PDF625檢視/開啟
    index.html0KbHTML1827檢視/開啟


    在CNU IR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