文化大學機構典藏 CCUR:Item 987654321/32148
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 46965/50831 (92%)
Visitors : 12654068      Online Users : 604
RC Version 6.0 © 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


    Please use this identifier to cite or link to this item: https://irlib.pccu.edu.tw/handle/987654321/32148


    Title: Anticolorectal cancer effects and pharmacokinetic application of 2, 2-Bis [4-(4-amino-3-hydroxyphenoxy) phenyl] adamantane
    Authors: Yang, Po-Sheng
    Wang, Jane-Jen
    Tsai, Tung-Hu
    Wang, Yea-Hwey
    Jan, Woan-Ching
    Cheng, Shih-Ping
    Chi, Chin-Wen
    Hsu, Yi-Chiung
    Contributors: 生科系
    Keywords: VIVO GROWTH-INHIBITION
    HUMAN COLON-CANCER
    IN-VITRO
    G(1) ARREST
    ERK PATHWAY
    CELL LINES
    DERIVATIVES
    P21(CIP/WAF1)
    ACTIVATION
    DIAMANTANE
    Date: 2015
    Issue Date: 2016-03-10 15:52:59 (UTC+8)
    Abstract: 2, 2-Bis (4-(4-amino-3-hydroxyphenoxy) phenyl) adamantane (DPA) induced growth inhibition in human cancer cells using the national cancer institute (NCI) anticancer drug screen. In our previous study, we demonstrated that DPA exerted growth inhibitory activities in the three human colon cancer cell lines (Colo 205, HT-29, and HCT-15). To identify the detailed mechanism, we examined the functional importance of p21 and p53 in DPA-induced anticancer effect. We used three isogenic colon cancer cell lines, HCT-116, HCT-116 p53(-/-), and HCT-116 p21(-/-), to evaluate the roles of p21 and p53 in the in vitro anticancer effects of DPA. DPA dose-dependently inhibited cell growth, cell migration and increased cell cycle at the G(0)/G(1) phase in HCT116 cells but not in p21(-/-) and p53(-/-) isogenic HCT-116 cells. Additionally, Western blot showed that DPA treatment induced the p21, p53, and cyclin-E protein expressions in HCT-116 cells. The p21 associated cell cycle regulatory protein such as cyclin D, CDK4, and pRb were decreased after DPA treatment in HCT-116 cells. DPA decreased cell migration in HCT-116 and HCT-116 p53(-/-) but not in HCT-116 p21(-/-) cells. We observed the up-regulation of E-cadherin, p-p38,and p-Erk in DPA-treated HCT-116 group but not in HCT-116 p21(-/-) and HCT-116 p53(-/-) groups. We assumed that p21 was required for DPA-induced anti-colon cancer effect through the Erk and p38 pathway leading to cell cycle arrest and inhibition of cell motility. Mean (+/- SE) pharmacokinetic parameters of the DPA were as follows: AUC = 64.44 +/- 8.41, Cmax = 1.56 +/- 0.48 and t(1/2) = 113.92 +/- 58.19. The pharmacokinetic data suggest DPA can be applied to further clinical study. This is the first pharmacokinetic study of DPA, and indicated that anti-proliferation and the cell mobility inhibition effects of DPA in HCT116 WT cells may result from the induction of p21 through activation of ERK and p38 pathway.
    Relation: INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE 卷: 8 期: 9 頁碼: 14805-14815
    Appears in Collections:[Department of Biology ] journal articles

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML644View/Open


    All items in CCUR are protected by copyright, with all rights reserved.


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