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    Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/10562


    Title: The novel p53-dependent metastatic and apoptotic pathway induced by vitexin in human oral cancer OC2 cells.
    Authors: Yang, SH
    Liao, PH
    Pan, YF
    Chen, SL
    Chou, SS
    Chou, MY
    Contributors: 中山醫學大學
    Keywords: PAI-1;PPARγ;apoptosis;metastasis;p53;vitexin
    Date: 2013
    Issue Date: 2015-03-30T09:54:40Z (UTC)
    ISSN: 0951-418X
    Abstract: Vitexin, identified as apigenin-8-C-D-glucopyranoside, a natural flavonoid compound found in certain herbs such as hawthorn herb, has been reported to exhibit anti-oxidative, anti-inflammatory, anti-metastatic and antitumor properties. The aim of this study was to investigate the possible existence of p53-dependent pathway underlying vitexin-induced metastasis and apoptosis in human oral cancer cells, OC2 cells. Vitexin decreased cell viability significantly. Meanwhile, the expression of tumor suppressor p53 and a small group of its downstream genes, p21(WAF1) and Bax, were upregulated. The p53 inhibitor pifithrin-α (PFT-α) knockdown of the signaling of p53 led vitexin to lose its antitumor effect and inhibited the expression of p53 downstream genes, p2(WAF1) and Bax. Vitexin had anti-metastatic potential accompanied with increasing plasminogen activator inhibitor 1 (PAI-1) accumulation and decreasing matrix metalloproteinase-2 expression. Our present study evidenced, by using p53 inhibitor PFT-α, PAI-1 and peroxisome proliferator-activated receptor γ are downstream genes of p53 in vitexin-induced signaling. MAPK inhibitor PD98059 decreased the OC2 cells viability significantly. The expression of p53 and its downstream genes p21(WAF1) and Bax were enhanced by blocking the activation of p42/p44 MAPK in response to treatment with vitexin. Moreover, p42/p44 MAPK played a negative role in p53-dependent metastasis and apoptosis. We give evidence for the first time that the novel p53-dependent metastatic and apoptotic pathway induced by vitexin in human oral cancer OC2 cells.
    Copyright © 2012 John Wiley & Sons, Ltd.
    URI: https://ir.csmu.edu.tw:8080/ir/handle/310902500/10562
    http://dx.doi.org/10.1002/ptr.4841
    http://dx.doi.org/10.1002/ptr.4841
    Relation: Phytother Res. 2013 Aug;27(8):1154-61.
    Appears in Collections:[牙醫學系暨碩士班] 期刊論文

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