Scientific Journal of

  Abstract

 Background and Objectives

 Arsenic trioxide ( As₂O₃ ) has been shown to have anti-cancer effects on a wide range of cancers. As₂O₃ has proved to be the most efficient in treatment of acute promyelocytic leukemia (APL) patients. It primarily acts by triggering apoptosis in cancer cells. To better understand the molecular mechanisms involved in As₂O₃ -induced apoptosis, in the present study we examined the effects of As₂O₃ both on the expression of Bax and Bcl-2 (the major regulators of apoptosis), and p53 genes in HL-60 cell line.

 Materials and Methods

 In this experimental study, the MTT colorimetric assay was used to assess the growth-inhibitory effect of As₂O₃ on HL-60 cells. The mRNA levels of p53, Bax and Bcl-2 were analyzed by using Real-time PCR. Data were analyzed by using SPSS18, t-test and ANOVA tests .

 Results

  As₂O₃ inhibits the growth of HL-60 cells in a dose dependent manner at 24h . Significant decrease (89% ± 3%) in cell viability was observed at 4μM and the IC50 value was about 16 μM. In HL-60 cell, no expression of p53 was detected. Real-time PCR results showed while Bax mRNA expression was not significantly affected in As₂O₃ treated HL-60, the Bcl-2/Bax ratio expression level significantly decreased in a dose dependent manner.

 Conclusions

  As₂O₃ exerts part of its antitumor effect by inducing apoptosis through decreasing Bcl-2/Bax mRNA ratio in p53-null leukemic cell line HL-60. More research on the protein level is required for these results to be reinforced.