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 [41]. Motsch et al. [42] 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 [43]. 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

of PRDM1 provides new insight into the genetic mechanisms underlying EN-NK/T-NT and an opportunity to identify new therapeutic strategies for EN-NK/T-NT. Acknowledgement This work was supported by the research grant 81071944 from National Natural Sciences Foundation of GSK458 nmr China, Beijing. References 1. Aozasa K, Takakuwa T, Hongyo T, Yang WI: Nasal NK/T-cell lymphoma: epidemiology and pathogenesis. Int J Hematol 2008, 87:110–117.PubMedCentralPubMedCrossRef 2. Ren YL, Nong L, Zhang S, Zhao J, Zhang XM, Li T: Analysis of 142 Northern Chinese patients with peripheral T/NK-Cell lymphomas: subtype distribution, clinicopathologic features, and prognosis. Am J Clin Pathol 2012, 138:435–447.PubMedCrossRef 3. Huang Y, de Reynies A, de Leval L, Ghazi

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