MicroRNA-34a promote apoptosis in T-cell acute lymphoblastic leukemia cell line (Jurkat)

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 TALL. 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, the flow cytometry assay was exploited to measure cell death and apoptosis stage. qPCR analyses showed that in Jurkat cells after transfection with miR-34a mimic (at the concentration of 5nmol) the expression of miR-34a mRNA was effectively increased compared with the 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 the concentration of 5nmol) was able to induce apoptosis in Jurkat cell line. 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.

Keywords:

Cancer , MiR-34a , Apoptosis , Jurkat cell line