English  |  正體中文  |  简体中文  |  Items with full text/Total items : 90074/105197 (86%)
Visitors : 7150854      Online Users : 46
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: http://asiair.asia.edu.tw/ir/handle/310904400/8258

    Title: Gallic Acid Induces Apoptosis via Caspase-3 and Mitochondrion-Dependent Pathways in Vitro and Suppresses Lung Xenograft Tumor Growth in Vivo
    Authors: Ji, BC (Ji, Bin-Chuan);Hsu, WH (Hsu, Wu-Huei);Yang, JS (Yang, Jai-Sing);Hsia, TC (Hsia, Te-Chun);Lu, CC (Lu, Chi-Cheng);Chiang, JH (Chiang, Jo-Hua);Yang, JL (Yang, Jiun-Long);Lin, CH (Lin, Ching-Hsiung);Lin, JJ (Lin, Jen-Jyh);Suen, LJW (Suen, Lee-Jen Wu);Wood, WG (Wood, Wellington Gibson);Chung, JG (Chung, Jing-Gung)
    Contributors: Department of Biotechnology
    Keywords: Gallic acid;apoptosis;caspase-3;mitochondria membrane potential (Delta Psi(m));NCI-H460 lung cancer cells;xenograft tumors
    Date: 2009-08
    Issue Date: 2010-03-26 10:29:23 (UTC+8)
    Publisher: Asia University
    Abstract: Several studies have shown that gallic acid (GA) induces apoptosis in different cancer cell lines, whereas the mechanism of action of GA-induced apoptosis at the molecular level in human non-small-cell lung cancer NCI-H460 cells is not well-known, Here, GA decreasing the percentage of viable NCI-H460 cells was investigated; GA-induced apoptosis involved G2/M phase arrest and intracellular Ca2+ production, the loss of mitochondrial membrane potential (Delta Psi(m)), and caspase-3 activation, The efficacious induction of apoptosis and DNA damage was observed at 50-500 mu M for 24 and/or 48 h as examined by flow cytometry, DAPI staining, and Comet assay methods. Western blotting and flow cytometric analysis also demonstrated that GA increased protein levels of GADD153 and GRP78, activation of caspase-8, -9, and -3, loss of Alp. and cytochrome c, and AIF release from mitochondria. Moreover, apoptosome formation and activation of caspase cascade were associated with apoptotic cell death. GA increased Sax and Bad protein levels and decreased Bcl-2 and Bcl-xL levels. GA may also induce apoptosis through a caspase-independent AIF pathway. In nude mice bearing NCI-H460 xenograft tumors, GA inhibited tumor growth in vivo. The data suggest that GA induced apoptosis In NCI-H460 lung cancer cells via a caspase-3 and mitochondrion-dependent pathway and inhibited the in vivo tumor growth of NCI-H460 cells in xenograft models.
    Appears in Collections:[生物科技學系] 期刊論文

    Files in This Item:

    File Description SizeFormat
    153.doc39KbMicrosoft Word548View/Open

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

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