Study on the apoptosis of Raji cell line induced by arsenic trioxide and its correlation with Survivin gene

Objective: To investigate the apoptosis induction by arsenic trioxide (As2O3) in Raji cells and its correlation with cell cycle arrest and expression of the Survivin gene. Methods: After Raji cells were treated with As2O3 in different concentrations (1, 2, 4 and 8 μM), for 24, 48 and 72 h, respectively, and cell proliferation was tested by MTT assay. Apoptosis was observed with electron microscope and DNA electrophoresis. The distribution of cell cycles and cell apoptosis were detected by flow cytometry. Expression of the Survivin gene was determined by real-time quantitative RT-PCR. Results: As2O3 (1–8 μM) inhibited Raji cells growth effectively in a dose- and time-dependent manner. As2O3 at 2–8 μM could induce cell apoptosis and cell cycle arrest. However, As2O3 (1 μM) inhibited Raji proliferation only by cell cycle arrest, without any symptoms of cell apoptosis. At the same time, Survivin gene expression was down-regulated after the treatment. Conclusion: As2O3 could induce substantial proliferation inhibition, cell cycle arrest and apoptosis in Raji cell. Cell cycle arrest might be a reason why apoptosis occurs. As2O3 can markedly down-regulate expression of the Survivin gene in a dose- and timedependent manner. The down-regulated Survivin gene might be leading to cell apoptosis by As2O3.

Objective： To investigate the apoptosis induction by arsenic trioxide （As2O3） in Raji cells and its correlation with cell cycle arrest and expression of the Survivin gene. Methods： After Raji cells were treated with As2O3 in different concen- trations （1, 2, 4 and 8 pM）, for 24, 48 and 72 h, respectively, and cell proliferation was tested by MTT assay. Apoptosis was observed with electron microscope and DNA electrophoresis. The distribution of cell cycles and cell apoptosis were detected by flow cytometry. Expression of the Survivin gene was determined by real-time quantitative RT-PCR. Results： As2O3 （1-8 μM） inhibited Raji cells growth effectively in a dose- and time-dependent manner. As2O3 at 2-8μM could induce cell apoptosis and cell cycle arrest. However, As2O3（1 μM） inhibited Raji proliferation only by cell cycle arrest, without any symptoms of cell apoptosis. At the same time, Survivin gene expression was down-regulated after the treatment. Conclusion： As2O3 could induce substantial proliferation inhibition, cell cycle arrest and apoptosis in Raji cell. Cell cycle arrest might be a reason why apoptosis occurs. As2O3 can markedly down-regulate expression of the Survivin gene in a dose- and timedependent manner. The down-regulated Survivin gene might be leading to cell apoptosis by As2O3.