ArticleExperimental and therapeutic medicine2021
MicroRNA-221 regulates cell activity and apoptosis in acute lymphoblastic leukemia via regulating PTEN.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Suppressing t(4;11) Acute Leukemia by Lipopolymer Nanoparticle Delivery of siRNA Targeting KMT2A::AFF1 with Enhanced Extrahepatic Delivery.Advanced healthcare materials · 2025Article
- MicroRNA in cancer therapy: breakthroughs and challenges in early clinical applications.Journal of experimental & clinical cancer research : CR · 2025Review
- Perspectives in MicroRNA Therapeutics for Cystic Fibrosis.Non-coding RNA · 2025Review
- Lipopolymer/siRNA Nanoparticles Targeting the Signal Transducer and Activator of Transcription 5A Disrupts Proliferation of Acute Lymphoblastic Leukemia.ACS pharmacology & translational science · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell acute lymphoblastic leukemia (T-ALL), an aggressive and heterogeneous malignancy originating from T cell precursors (thymocytes), accounts for ~15% of all ALL cases in children and for ~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.
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