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    標題: Rugosin E, an ellagitannin, inhibits MDA-MB-231 human breast cancer cell proliferation and induces apoptosis by inhibiting nuclear factor-kB signaling pathway
    Rugosin E,鞣花單寧酸,透過抑制NF-kB路徑而抑制人類乳癌細胞MDA-MB-231的細胞增生並誘導細胞凋亡
    作者: Yin-Yi Chen(陳胤伊)
    Ya-Ling Hsu(許雅玲)
    Ta-Chen Lin(林大楨)
    Wen-Sheng Tzeng(曾文盛)
    Chun-Ching Lin(林俊清)
    Po-Lin Kuo(郭柏麟)
    貢獻者: Department of Biotechnology, Chia-Nan University of Pharmacy and Science
    Center of General Education, Central Taiwan University of Science and Technology
    Attending Diagnostic Radiologist, Chi-Mei Foundation Hospital, Tainan
    日期: 2008-07
    上傳時間: 2017-12-04 15:59:59 (UTC+8)
    摘要: Background and Purpose: We used a human breast cancer cell line, MDA-MB-231, to evaluate the potential of rugosin E as a chemopreventive agent against breast cancer. Methods: Cell proliferation assay (XTT); Cell cycle analysis (Flow cytometer); Apoptosis analysis; Caspase activity assay; Western blotting assay; Electrophoretic mobility shift assay (EMSA); NF-kb receptor assay; RT-PCR analysis. Results: Treatment with rugosin E decreased the cell proliferation of MDA-MB-231 cells in a dose-dependent manner and arrested MDA-MB-231 cells at G0/G1 phase. This effect was strongly associated with concomitant decrease in the level of cyclin D1, cyclin D2, cyclin E, cdk2, cdk4, and cdk6, and increase of p21/WAF1. In addition, rugosin E also induced apoptotic cell death. Rugosin E increased in the expression of Bax, Bak, and Bcl-Xs, but decreased the levels of Bcl-2 and Bcl-XL, and subsequently triggered mitochondria apoptotic pathway (release of cytochrome c, activation of caspase-9, and caspase-3). In addition, pre-treatment of cells with caspase-9 inhibitor blocked rugosin E-induced cell proliferation and apoptosis, indicating caspase-9 activation was involved in rugosin E-mediated MDA-MB-231 cells apoptosis. Rugosin E inhibited the constitutively activated and inducible NF-kb in both its DNA-binding activity and transcriptional activity. Furthermore, rugosin E also inhibited the TNF- -activated NF-kB-dependent reporter gene expression of cyclin D1, c-Myc, XIAP, Bcl-2, and Bcl-XL were all downregulated by rugosin E. Conclusions: Our results indicated that rugosin E inhibits the activation of NF-kB, and this may provide a molecular basis for drug development in the prevention and treatment of cancer by rugosin E.
    Appears in Collections:[藥理學院] 2008第五屆海峽化學、生物及材料研討會
    [生物科技系(所)] 會議論文

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