English  |  正體中文  |  简体中文  |  Items with full text/Total items : 17938/22957 (78%)
Visitors : 7403556      Online Users : 148
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
    Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/15607


    Title: Delphinidin-rich extracts of Hibiscus sabdariffa L. trigger mitochondria-derived autophagy and necrosis through reactive oxygen species in human breast cancer cells
    Authors: Wu, C.-H.
    Huang, C.-C.
    Hung, C.-H.
    Yao, F.-Y.
    Wang, C.-J.
    Chang, Y.-C.
    Contributors: 醫學研究所
    Keywords: Anthocyanins;Autophagy;Breast cancer;Hibiscus sabdariffa L.;Necrosis;Reactive oxygen species
    Date: 2016-08-01
    Issue Date: 2016-08-04T03:34:53Z (UTC)
    Publisher: Elsevier Ltd
    ISSN: 17564646
    Abstract: Anthocyanins from Hibiscus sabdariffa L. (HAs) possess anticancer potential and diverse biological effects, but its correlation with human breast cancer cells and different modes of cell death is unclear. Here, we show that HAs can induce both autophagy and necrosis cell death distinct from apoptosis in MCF-7 cells. HAs could effectively reduce the viability of MCF-7 cells. Unexpectedly, HAs failed to stimulate the apoptosis-related proteins Bcl2 and Bax. Autophagy was characterized by acridine orange staining, LC3 (light chain 3) activation and AMPK (AMP-activated kinase) phosphorylation. The necrosis death was confirmed by annexin V/propidium iodide (PI) double-positive detection and PI uptake assay. HAs-elicited responses were accompanied by reactive oxygen species (ROS) elevation and mitochondrial membrane potential collapse. Moreover, N-acetylcysteine (NAC) reversed HAs induced cell viability. Our study is the first to report that HAs-modified mitochondrial function triggers cell death by autophagy and necrosis in MCF-7 cells rather than programmed cell death. © 2016 Elsevier Ltd.
    URI: https://ir.csmu.edu.tw:8080/ir/handle/310902500/15607
    http://dx.doi.org/10.1016/j.jff.2016.05.018
    Relation: Journal of Functional Foods Volume 25, 1 August 2016, Pages 279-290
    Appears in Collections:[醫學研究所] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML420View/Open


    SFX Query

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


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