ArticleGalen medical journal2025
Investigating the Impact of LNA-anti-miR-92b, miR-181b, TNF-α, and Piperine on Gene Expression and Cell Viability in Jurkat Cells: Implications for Acute Lymphoblastic Leukemia : LNA-anti- MicroRNAs and Jurkat Cells.
Article in Galen medical journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Dysregulated Expression of miR-222 and miR-15a in Transfusion-Dependent Thalassemia: Associations with Torque Teno Virus and Cytomegalovirus Infections.International journal of hematology-oncology and stem cell research · 2025Article
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5 authors.
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Abstract
Background: Acute lymphoblastic leukemia/lymphoblastic lymphoma (ALL/LBL), a prevalent pediatric cancer, arises from precursor lymphoid cells and is affected by various risk factors. Abnormal microRNAs (miRs) and dysregulated expression of BCL-2 family proteins significantly contribute to leukemogenesis. Piperine, noted for its anti-tumor capabilities, has demonstrated potential in enhancing the sensitivity of cancer cells to treatment. We aimed in this study to investigate the influence of specific miRs (miR-92b, miR-181b) and TNF-α on the proliferation and viability of the Jurkat cell line, and examined the effects of piperine on miR expression and the genes BAX, BCL-2, and MCL-1. Materials and Methods: Jurkat T-cells were cultured and treated with LNA-miR inhibitors to selectively suppress miR-181b and miR-92b expression. Cell viability was assessed using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay, while miR-92b, miR-181b, MCL-1, BAX, and BCL-2 mRNA levels were quantified using SYBR Green Real-Time PCR (Polymerase Chain Reaction). SPSS software (version 18) was utilized for statistical analysis. Results: The study demonstrated effective inhibition of miR-181b and miR-92b through LNA-anti-miR technology. Treatment with LNA-anti-miR-92b and TNF-α reduced Jurkat cell survival, whereas inhibiting miR-181b enhanced viability. BAX expression decreased with LNA-anti-miR-181b and piperine treatment, while BCL-2 expression declined with LNA-anti-miR-92b and piperine treatment. Additionally, piperine treatment increased miR-181b expression while reducing miR-92b and TNF-α expression. Conclusion: Our findings suggest that inhibiting miR-92b, miR-181b, TNF-α, and BAX using LNA-anti-miR could be a promising strategy for treating ALL. Piperine may enhance this approach by upregulating BAX. Further research is needed to explore these possibilities and develop effective treatments.
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