ASIA unversity:Item 310904400/86690
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 94286/110023 (86%)
Visitors : 21654576      Online Users : 899
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/310904400/86690


    Title: Phenethyl isothiocyanate triggers apoptosis in human malignant melanoma A375.S35 cells through reactive oxygen species and the mitochondria-dependent pathways
    Authors: 鄭揚耀、王明昌、蔡宜靜, 張眾卓(Chong-Chuo Chang)
    Contributors: 財務金融學系
    Keywords: A375.S2 melanoma cells;PEITC;ROS;apoptosis;mitochondria
    Date: 2014
    Issue Date: 2014-10-30 07:31:48 (UTC+0)
    Abstract: We have reported previously that phenethyl isothiocyanate (PEITC) induces apoptosis in human osteosarcoma U-2 OS cells. Cytotoxic activity of PEITC towards other cancer cells such as human malignant melanoma and skin cancer cells has not been reported. In this study, the anticancer activity of PEITC towards human malignant melanoma cancer A375.S2 cells was investigated. To determine the mechanisms of PEITC inhibition of cell growth, the following end points were determined in A375.S2 cells: cell morphological changes, cell cycle arrest, DNA damage and fragmentation assays and morphological assessment of nuclear change, reactive oxygen species (ROS) and Ca(2+) generations, mitochondrial membrane potential disruption, and nitric oxide and 10-N-nonyl acridine orange productions, expression and activation of caspase-3 and -9, B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), Bcl-2, poly (adenosine diphosphate-ribose) polymerase, and cytochrome c release, apoptosis-inducing factor and endonuclease G. PEITC induced morphological changes in time- and dose-dependent manner. PEITC induced G2/M phase arrest and induced apoptosis via endoplasmic reticulum stress-mediated mitochondria-dependent pathway. Western blot analysis showed that PEITC promoted Bax expression and inhibited Bcl-2 expression associated with the disintegration of the outer mitochondrial membrane causing cytochrome c release, and activation of caspase-9 and -3 cascade leading to apoptosis. We conclude that PEITC-triggered apoptotic death in A375.S2 cells occurs through ROS-mediated mitochondria-dependent pathways.
    Relation: 證券市場發展季刊/Review of Securities and Futures Markets;33(3):270-83.
    Appears in Collections:[Department of Finance] Journal Article

    Files in This Item:

    File SizeFormat
    index.html0KbHTML348View/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