Scientific Journal of

  Abstract

 Background and Objectives

 Acute promyelocytic leukemia (APL) is one of the most malignant forms of acute leukemia with a fatal course of only weeks which represents 10-15% of AML in adults. Arsenic trioxide as a single agent factor (without chemotherapy) is the treatment of choice for APL patients it induces cell death through apoptosis but the mechanism by which arsenic targets apoptosis and dramatically affects gene expression remains poorly understood. Since arsenic is used as first line treatment in Iran, it is worth investigating its effect on expression of genes involved in APL.

 Materials and Methods

 In this descriptive study, to understand the underlying mechanisms of cell death induction by arsenic, we treated NB4 cell line in a dose and time dependent manner. Extracting RNA and synthesis of cDNA, gene expression of apoptotic genes in mitochondrial pathway including caspase3, Mcl-1 and Bcl-2 was analyzed through Real-Time PCR.

 Results

 Our findings showed that As₂O₃-induced cell death was paralleled by reduced expression of the antiapoptotic protein Bcl-2 but the expression of Caspase3 and Mcl-1 did not change after arsenic treatment.

 Conclusions

 These results suggest that changes in Bcl-2 gene expression may be one of the mechanisms of action of arsenic in induction of apoptosis, while Caspase3 and Mcl-1 gene expression are not affected by arsenic at the transcriptional level.

 Key words : Promyelocytic Leukemia, Acute, arsenic trioxide, Apoptosis, Caspase 3, bcl-2 Genes