MicroRNA-221 regulates cell activity and apoptosis in acute lymphoblastic leukemia via regulating PTEN

T cell acute lymphoblastic leukemia (T-ALL), an aggressive and heterogeneous malignancy originating from T cell precursors (thymocytes), accounts for similar to 15% of all ALL cases in children and for similar to 25% in adults. The present study aimed to investigate the role of microRNA-221 (miR-221) in the regulation of cell viability and apoptosis of human T-ALL cells and its related regulatory mechanisms. To perform this investigation, miR-221 was upregulated or knocked down in human T-ALL cells (Jurkat cells) using miR-221 mimic or inhibitor, respectively. Then, cell viability was determined using a 3-(4,5-dimethylthiahiazol-2-y1)-2,5-diphenytetrazolium bromide assay, cell invasion and migration were analyzed via Transwell assays, and cell apoptosis was detected using flow cytometry. It was found that transfection with a miR-221 inhibitor significantly inhibited Jurkat cell viability, migration and invasion, and induced Jurkat cell apoptosis. Whereas, transfection with the miR-221 mimic resulted in the opposite effects. Besides, the results showed that phosphatase and tensin homologue deleted on chromosome 10 (PTEN) was a target of miR-221. Moreover, it was observed that the effects of the miR-221 inhibitor on Jurkat cell viability, migration and invasion, and cell apoptosis were significantly eliminated by PTEN-small interfering RNA. In addition, it was shown that the phosphatidylinositol 3-kinase/AKT pathway was involved in the effect of miR-221 on Jurkat cells. In conclusion, the data indicated that miR-221 existed as an oncogene in T-ALL, and its downregulation could inhibit the development of ALL by targeting PTEN. Therefore, miR-221 may be a novel potential therapeutic target for ALL.

Automated summary

The study revealed that miR-221 acts as an oncogene in T-ALL, and its downregulation inhibits the development of ALL by targeting PTEN. Therefore, miR-221 may serve as a potential novel therapeutic target for ALL.