Objective:To explore the effects of arsenic trioxide (ATO) on the apoptosis of glucocorticoid (GC)-resistant T-acute lymphoblastic leukemia (ALL) CEM-C1 cells and its possible mechanisms. Methods:Different concentrations of ATO (0.25 μmol/L?5 μmol/L) were used to induce the apoptosis of CEM-C1 cells. The inhibition rate of cell proliferation and apoptosis were detected by MTT test,Annexin V-FITC/PI flow cytometry and optical microscopy,respectively. RT-PCR was applied to semi-quantitatively analyze the mRNA expression of pro-apoptotic proteins (Bad and PDCD4) and anti-apoptotic proteins (XIAP and MCL-1) induced by different concentrations of ATO at different time points. Results:ATO could inhibit proliferation and induce apoptosis of CEM-C1 cells at a concentration and time dependent manner. Low-dose ATO mildly inhibited the proliferation of CEM-C1 cells while higher concentrations (1 μmol/L and 5 μmol/L) had strong anti-tumor effect with the inhibiting rates of 40.07±7.98% and 88.67±2.88%,respectively. Annexin V-FITC/PI flow cytometry showed that the apoptotic rates of CEM-C1 cells were significantly increased after 48 hours treatment of different concentrations of ATO. RT-PCR demonstrated up-regulated mRNA expression of pro-apoptotic protein Bad and PDCD4 but down-regulated mRNA expression of anti-apoptotic protein XIAP when CEM-C1 cells were treated with different concentrations of ATO at different time points. The MCL-1 mRNA expression was down-regulated only after the treatment of 5 μmol/L ATO. Conclusion:ATO can inhibit cell proliferation and induce cell apoptosis in GC-resistant CEM-C1 cells. The molecular mechanisms might involve the increased mRNA expression of pro-apoptotic protein Bad and PDCD-4,and rapid down-regulation of XIAP mRNA expression. Objective: To explore the effects of arsenic trioxide (ATO) on the apoptosis of glucocorticoid (GC) -resistant T-acute lymphoblastic leukemia (ALL) CEM-C1 cells and its possible mechanisms. Methods: Different concentrations of ATO (0.25 μmol / L ? 5 μmol / L) were used to induce the apoptosis of CEM-C1 cells. The inhibition rate of cell proliferation and apoptosis were detected by MTT test, Annexin V-FITC / PI flow cytometry and optical microscopy, respectively. RT-PCR was applied to semi-quantitatively analyze the mRNA expression of pro-apoptotic proteins (Bad and PDCD4) and anti-apoptotic proteins (XIAP and MCL-1) induced by different concentrations of ATO at different time points. Low-dose ATO mildly inhibited the proliferation of CEM-C1 cells while higher concentrations (1 μmol / L and 5 μmol / L) had strong anti-tumor effect with the inhibiting rates of 40.07 ± 7.98% and 88 .67 ± 2.88%, respectively. Annexin V-FITC / PI flow cytometry showed that the apoptotic rates of CEM-C1 cells were significantly increased after 48 hours treatment of different concentrations of ATO. RT-PCR demonstrated up-regulated mRNA expression of pro -APoptotic protein Bad and PDCD4 but down-regulated mRNA expression of anti-apoptotic protein XIAP when CEM-C1 cells were treated with different concentrations of ATO at different time points. The MCL-1 mRNA expression was down-regulated only after the treatment of 5 μmol / L ATO. Conclusion: ATO can inhibit cell proliferation and induce cell apoptosis in GC-resistant CEM-C1 cells. The molecular mechanisms might involve the increased mRNA expression of pro-apoptotic protein Bad and PDCD-4, and rapid down- regulation of XIAP mRNA expression.