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.