Thallium acetate induces C6 glioma cell apoptosis

Chee Fah Chia, Soul-Chin Chen, Chin Shyang Chen, Chuen Ming Shih, Horng Mo Lee, Chih Hsiung Wu

研究成果: 雜誌貢獻文章同行評審

22 引文 斯高帕斯(Scopus)


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 G 2/M phase and caused cellular apoptosis at 300 μM 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 p21Cip1, but not p27Kip1. 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 p21Cip1. 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.
頁(從 - 到)523-530
期刊Annals of the New York Academy of Sciences
出版狀態已發佈 - 2005

ASJC Scopus subject areas

  • 生物化學、遺傳與分子生物學 (全部)
  • 科學史與哲學


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