رضا محمد زاده

Background: T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive lymphoid malignancy due to the oncogenic transformation of immature T-cell progenitors. The emergence of microRNAs as gene expression regulators identifies them as emerging diagnostic candidates and potential therapeutic targets. microRNAs play a crucial role in the progression of T-ALL by regulating proliferation and apoptosis through targeting major signaling pathways or transcription factors. miR-34a is a tumor suppressor with reduced expression levels in many cancers, including T-ALL. The purpose of the present study was to investigate the effect of miR-34a on induction of apoptosis in the jurkat cell line. Methods: Jurkat cells which are related to T-cell acute lymphoblastic leukemia (T-ALL) were cultured in RPMI1640 medium supplemented with 10% fetal bovine serum (FBS) at 37˚C and 5% CO2. miR-34a mimic was transfected using jetPEI in vitro DNA transfection reagent and the expression of miR-34a was detected using quantitative real-time PCR. Cell viability of jurkat cells was detected using 3-(4, 5-dimethylthiazol-2-yl)- 2, 5-diphenyltetrazolium bromide (MTT) assay. Then, flow cytometry assay was exploited measure the percentage of apoptotic cells. Finally, Cell cycle assay was used to differentiate different phases of the cell cycle. Results: qRT-PCR analyses showed that in Jurkat cells after transfection with miR-34a mimic at the concentration of 5nmol the expression of miR-34a mRNA was significantly increased compared to the control group. MTT assay results demonstrated that transfection by miR-34a at the concentration of 5nmol decreased the viability of jurkat cells and reduction in cell viability obeyed a dose-dependent course. According to the flow cytometry assay result, in the transfected cells, miR-34a mimic at the concentration of 5nmol was able to induce apoptosis the in Jurkat cell line. Data derived from cell cycle assay revealed that cell cycle arrest in cancer cells which hav