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    請使用永久網址來引用或連結此文件: http://libir.tmu.edu.tw/handle/987654321/13625


    題名: Thallium Acetate Induces C6 Glioma Cell Apoptosis.
    作者: 吳志雄
    Chia CF;Chen SC;Chen CS;Shih CM;Lee HM;Wu CH
    貢獻者: 醫學系外科學科
    日期: 2005
    上傳時間: 2009-10-28 12:26:26 (UTC+8)
    摘要: Thallium acetate is a known neurotoxic agent. In this study, we investigated the mechanisms by which thallium acetate induces cell cycle arrest and cell apoptosis in cultured LC6 glioma cells. Exposure of C6 glioma cells to thallium acetate decreased cell viability as demonstrated by the MTT assay. Incubation of thallium acetate arrested cell cycle progression at the G2/M phase and caused cellular apoptosis at 300 microM as determined by trypan blue exclusion and flow cytometric analysis. The G2/M arrest was associated with a decrease in expression of CDK2 protein and an upregulation of p53 and the CDK inhibitor p21(Cip1), but not p27(Kip1). Thallium acetate did not alter the protein levels of cyclin A and B; cyclin D1, D2, and D3; and CDK4 expression in C6 glioma cells. Incubation of C6 glioma cells with thallium acetate upregulated the expression of proapoptotic proteins Bad and Apaf and downregulated the expression of anti-apoptotic proteins Bcl-xL and Bcl-2. In conclusion, these data suggest that thallium acetate inhibits cell cycle progression at G2/M phase by suppressing CDK activity through the p53-mediated induction of the CDK inhibitor p21(Cip1). Impairment of cell cycle progression may trigger the activation of a mitochondrial pathway and shifts the balance in the Bcl-2 family toward the proapoptotic members, promoting the formation of the apoptosome and, consequently, apoptosis.
    關聯: Annals of the New York Academy of Sciences.(1042):523-530.
    資料類型: article
    顯示於類別:[外科學科] 期刊論文

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