國家衛生研究院 NHRI:Item 3990099045/14477
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 12189/12972 (94%)
造訪人次 : 965998      線上人數 : 669
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/3990099045/14477


    題名: Caffeic acid phenethyl ester suppresses drug resistance of enzalutamide or abiraterone in prostate cancer cells
    作者: Chuu, CP;Kuo, YY;Huo, C
    貢獻者: Institute of Cellular and Systems Medicine
    摘要: Enzalutamide (ENZ) and Abiraterone acetate (AA) are drugs targeting androgen receptor axis for treatment of metastatic castration-resistant prostate cancer (mCRPC). However, a majority of patients receiving these treatments will eventually acquire drug resistance, which is caused by multiple mechanisms including the activation of AR splice variant 7 (AR-V7). We determined if caffeic acid phenethyl ester (CAPE) can suppress the signaling of AR-V7 and tumor growth of ENZ-resistant or AA-resistant mCRPC cells. CAPE treatment dose-dependently suppressed the transcriptional activity of AR-V7, its target gene UBE2C and TMPRSS2, and its splicing factors U2AF65, SF2 and HNRNPF. Cyclohexamide treatment and MG132 treatment revealed that stability of AR-V7 was reduced by CAPE and CAPE increased AR-V7 tagged for the proteasomal degradation. Fluorescence microscopy demonstrated that treatment with CAPE reduced nuclear accumulation of AR-V7 as well as phosphorylation of Ser81 and Ser213 on AR-V7, which decreases the stability and abundance of AR-V7. CAPE inhibits the expression of CDK1 and AKT, the two kinases phosphorylating Ser81 and Ser213 on AR, respectively. Overexpression of CDK1, AKT, or c-Myc rescued the AR-V7 protein level under CAPE treatment. Injection of CAPE repressed tumor growth of 22Rv1 xenografts as well as AR-V7, CDK1 and AKT expression in tumors. Combined treatment of CAPE and ENZ or AA suppress the proliferation of enzalutamide-resistant or Abiraterone-resistant CRPC cells via inhibition of AR-V7. Our results suggested that CAPE treatment reduced expression level, stability and transcriptional activity of AR-V7 in CRPC cells, and thus prevented implying the development of resistance against enzalutamide and abiraterone via inhibition of AR-V7. CAPE may be a promising therapeutic agent for enzalutamide-resistant or abiraterone-resistant CRPC.
    日期: 2022-07
    關聯: Annals of Oncology. 2022 Jul;33(Suppl. 6):S493-S494.
    Link to: http://dx.doi.org/10.1016/j.annonc.2022.05.148
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0923-7534&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000834940400248
    顯示於類別:[褚志斌] 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
    ISI000834940400248.pdf123KbAdobe PDF110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