中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/1978
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    CMUR > College of Medicine > School of Medicine > Journal articles >  Item 310903500/1978
    Please use this identifier to cite or link to this item: http://ir.cmu.edu.tw/ir/handle/310903500/1978


    Title: Differential regulation of activator protein 1 activity by glycyrrhizin.
    Authors: 項千芸(Chien-Yun Hsiang);賴羿如(I-Lu Lai);趙德澂(De-Cheng Chao);侯庭鏞(Tin-Yun Ho)*
    Contributors: 醫學院醫學系學士班微生物學科
    Keywords: Activator protein 1;Glycyrrhizin;Tumor promotion
    Date: 2002-02
    Issue Date: 2009-08-19 17:23:26 (UTC+8)
    Abstract: Glycyrrhizin, a major component of Glycyrrhiza uralensis (licorice) root, is a saponin and exhibits a number of pharmacological effects, including anti-inflammation, anti-ulcer, anti-allergy, and anti-carcinogenesis. Activator protein 1 (AP-1), a nuclear transcription factor, consists of Jun/Fos heterodimers or Jun/Jun homodimers, and blocking of tumor promoter-induced AP-1 activity could inhibit induced cellular transformation. In order to elucidate the molecular mechanism of glycyrrhizin-induced anticarcinogenesis, effect of glycyrrhizin on the AP-1 activity in untreated and tumor promoter—12-O-tetradecanoylphorbol-13-acetate (TPA)-treated conditions was analyzed in this study. Glycyrrhizin induced the AP-1/TATA reporter activity in a dose-dependent fashion, which was judged by chloramphenicol acetyltransferase assay and electrophoretic mobility-shift assay. Similar results were observed in HepG2 and Vero cells, suggested that glycyrrhizin effect was cell type-independent. In addition, the cis element responsible for glycyrrhizin activity was AP-1 responsive element. Further analysis indicated that glycyrrhizin exhibited a different regulation on the AP-1 activity in untreated and TPA-treated cells. Glycyrrhizin induced the AP-1 activity in untreated cells, while it inhibited the TPA-induced AP-1 activation in TPA-treated cells. These results provide insight into the biological actions of glycyrrhizin and the molecular basis for the development of new chemoprotective agents for cancer.
    Relation: LIFE SCIENCES 70(14):1643~1656
    Appears in Collections:[School of Medicine] Journal articles

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