رضا محمد زاده

Background: T-cell acute lymphoblastic leukemia is a lymphoid malignancy affected by oncogenic transformation of immature T-cell progenitors. Acute lymphoblastic leukemia currently accounts for 20-25% of adults and 10-15% of pediatric cases. Clinically, T-ALL patients represent high white blood cell counts. MicroRNAs are a class of small, highly conserved non-coding RNAs containing ~22 nucleotides that interact with the mRNAs of coding genes to direct their post-transcriptional repression. miR-34a is a tumor suppressor with lost or reduced levels of expression in many cancers, including T-ALL. Method: Jurkat T-cell acute lymphoblastic leukemia (T-ALL) cells were maintained in RPMI 1640. miR-34a mimic was transfected using jetPEI in vitro DNA transfection reagent. Cell viability was assessed with 3-(4, 5-dimethylthiazol-2-yl)- 2, 5-diphenyltetrazolium bromide (MTT) assay. Total RNA was extracted from the cells by using TRIzol reagent. Then, flow cytometry assay was exploited to measure cell death and apoptosis stage. Results: qPCR analyses showed that in Jurkat cells after transfection with miR-34a mimic (at concentration of 5nmol) the expression of miR-34a mRNA was effectively increased compared with control group. MTT assay results of microRNA were dose-dependent and at the 5nmol concentration of miR-34a, cell viability was less than their value in the control group. According to the flow cytometry assay result, in the transfected cells, miR-34a mimic (at concentration of 5nmol) was able to induce apoptosis in Jurkat cell line. Conclusion: Our results suggest that the miR-34a effectively decreases the viability of T-cell acute lymphoblastic leukemia cells, induces apoptosis in this cell line, and therefore could be considered as a potent adjuvant in T-ALL therapy.