Asma Vafadar - Department of Medical Biotechnology, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran
Niloufar Nazemoroaya - Department of Basic Science, School of Medicine, Faculty of molecular Genetics, Science and Research Branch, Islamic Azad University, Tehran, Iran
Gholamhossein Tamaddon - Diagnostic Laboratory Sciences and Technology Research Center, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran

Precursor B-cell acute lymphoblastic leukemia (B-ALL) is the most prevalent pediatric cancer. DNA methylation and changes in the microRNAs expression of are known to be important causes of B-ALL. Decitabine as a DNA methyltransferase inhibitor agent is able to induce hypomethylation in several tumor suppressor genes. Much evidence has proven BTG2 act as tumor suppressor gene in many malignancies. In the current study, the mRNA expression of BTG2 gene using qReal-time PCR in Nalm6 cell line and five patients suffer from ALL with mean age 5.6 years were determined in compare with seven normal healthy donors age and sex matched. Quantitative Real-time PCR analysis revealed that the expression levels of BTG2 gene was significantly decreased in Nalm6 and according to the Methylation specific PCR (MSP) analysis, this gene was hypermethylated in Nalm6. In next step, the effects of decitabine treatment on the methylation and expression of this gene in association with changes in miR-125b expression levels was evaluated in optimal concentration 2.5 μM of decitabine. Our data showed that decitabine is able to restore the expression level of mentioned gene and down regulate expression level of oncomir 125b in Nalm6 cell line. Therefore, it seems that decitabine can be used as a potential drug for the first line treatment of B-ALL patients, but further in vivo investigation is necessary.

B-ALL, DNA methylation, MicroRNA, Decitabine, NALM6