miRNA-155 Modulates the Malignant Biological Characteristics of NK/T-Cell Lymphoma Cells by Targeting FOXO3a Gene

2014 
This study investigated the effects of mi RNA-155 on malignant biological characteristics of NK/T-cell lymphoma cell lines and the possible mechanism. The expression of mi RNA-155 was detected in lymphoma cell lines from different sources(SNK-6, YTS, Jurkat and DOHH2) by real-time PCR. Lentiviral vectors(p LL3.7) that could overexpress or downexpress mi RNA-155 were constructed. Recombinant lentiviral particles were prepared and purified, and their titers determined. The expression of mi RNA-155 in the infected SNK-6 cells and the cell proliferation were detected by PCR and CCK-8, respectively. Flow cytometry was used to determine the apoptosis of infected SNK-6 cells. The target of mi RNA155 was predicted from Targetscan website. The effect of mi RNA155 on FOXO3 a expression was examined by Western blotting. The results showed that among the human NK/T-cell lymphoma cell lines SNK-6, YTS, Jurkat and DOHH2, the expression of mi RNA-155 was highest in SNK-6. The infection efficiency of the recombinant lentivirus in SNK-6 was more than 70% at multiplicity of infection(MOI) of 100. The expression of mi RNA-155 was significantly increased in SNK-6 cells infected by lentivirus vectors with high expression of mi RNA-155(4 times higher than the control group), and profoundly decreased in those infected with lentiviruses with low expression of mi RNA-155. The proliferation of letivirus-infected SNK-6 cells was decreased as the expression of mi RNA-155 reduced. The apoptosis rate was increased with the reduction in the expression of mi RNA-155. FOXO3 a was found to be a possible target of mi RNA155, as suggested by Targetscan website. Western blotting showed that the expression of FOXO3 a was significantly elevated in SNK-6 cells with mi RNA-155 inhibition. It was concluded that reduction in mi RNA-155 expression can inhibit the proliferation of SNK-6 lymphoma cells and promote their apoptosis, which may be associated with regulation of FOXO3 a gene.
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