In our study, all miR-223-positive cases of EN-NK/T-NT showed EBV infection, implying that EBV infection may be responsible for miR-223 overexpression. Indeed, the upregulation of miR-223 has been observed after EBV transformation of lymphoblastoid cells . Motsch et al.  also demonstrated that EBV exerts a profound find more effect on the cellular miRNA profile in EBV-positive NK/T-cell lymphomas compared to non-infected cases. Other reports have revealed that CCAAT/enhancer binding protein alpha and nuclear factor I/A regulate mature miR-223 by competing for a regulatory binding site 700 bp Pritelivir in vitro upstream of the pre-miR-223
sequence . Thus, the mechanisms that regulate the level of miR-223 remain to be elucidated. Conclusions Collectively, these findings in our study indicate that PRDM1 is downregulated in EN-NK/T-NT cases and that PRDM1-positive staining may have prognostic value for evaluating the prognosis for EN-NK/T-NT patients. In addition, PRDM1 is likely to be a target of miR-223, and the overexpression of miR-223 might be an important genetic mechanism of PRDM1 downregulation in EN-NK/T-NT. miR-223-mediated silencing
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