Taipei Medical University Institutional Repository:Item 987654321/3797
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    Please use this identifier to cite or link to this item: http://libir.tmu.edu.tw/handle/987654321/3797


    Title: Theanaphthoquinone inhibits fatty acid synthase expression in EGF-stimulated human breast cancer cells via the regulation of EGFR/ErbB-2 signaling
    Authors: 何元順
    Meng-Shih Weng;Chi-Tang Ho;Yuan-Soon Ho;Jen-Kun Lin
    Contributors: 醫學檢驗暨生物技術學系
    Keywords: Mammary gland diseases;Enzyme;Transferases;Acyltransferases;Transcription factor SREBP1;Breast cancer;Anticarcinogen;Protooncogene;C-Onc gene;erbB2 Gene;Signal transduction;Malignant tumor;Epidermal growth factor receptor;Tumor cell;Human;Epidermal growth factor;Fatty-acid synthase;Enzyme inhibitor
    Date: 2007
    Issue Date: 2009-08-25 10:39:09 (UTC+8)
    Abstract: Fatty acid synthase (FAS) is a major lipogenic enzyme catalyzing the synthesis of long-chain saturated fatty acids. Most breast cancers require
    lipogenesis for growth. Here, we demonstrated the effects of theanaphthoquinone (TNQ), a member of the thearubigins generated by the oxidation
    of theaflavin (TF-1), on the expression of FAS in human breast cancer cells. TNQ was found to suppress the EGF-induced expression of FAS
    mRNA and FAS protein in MDA-MB-231 cells. Expression of FAS has previously been shown to be regulated by the SREBP family of
    transcription factors. In this study, we demonstrated that the EGF-induced nuclear translocation of SREBP-1 was blocked by TNQ. Moreover,
    TNQ also modulated EGF-induced ERK1/2 and Akt phosphorylation. Treatment of MDA-MB-231 cells with PI 3-kinase inhibitors, LY294002
    and Wortmannin, inhibited the EGF-induced expression of FAS and nuclear translocation of SREBP-1. Treatment with TNQ inhibited EGFinduced
    EGFR/ErbB-2 phosphorylation and dimerization. Furthermore, treatment with kinase inhibitors of EGFR and ErbB-2 suggested that
    EGFR/ErbB-2 activation was involved in EGF-induced FAS expression. In constitutive FAS expression, TNQ inhibited FAS expression and Akt
    autophosphorylation in BT-474 cells. The PI 3-kinase inhibitors and tyrosine kinase inhibitors of EGFR and ErbB-2 also reduced constitutive FAS
    expression. In addition, pharmacological blockade of FAS by TNQ decreased cell viability and induced cell death in BT-474 cells. In summary,
    our findings suggest that TNQ modulates FAS expression by the regulation of EGFR/ErbB-2 pathways and induces cell death in breast cancer
    cells.
    Relation: Toxicology and Applied Pharmacology.(218):107-118.
    Data Type: article
    Appears in Collections:[ ] Periodical Articles

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