0%, 6.0%, and 9.3% of YT cells, respectively. Similarly, both qRT-PCR and western blot analysis revealed the discrepancy between PRDM1 transcript and its protein in some NK/T-cell www.selleckchem.com/products/EX-527.html lymphoma cell lines. As shown in Figure 2B and Figure 2C, in contrast to YT or NK92 cells, QNZ which presented consistent levels in both transcription and protein of PRDM1, PRDM1 transcripts in NKL cells are estimated at about 73.0% of those in YT cells (Figure 2B), whereas PRDM1α protein is just 6.0% (Figure 2C). Similarly, PRDM1α transcript and protein levels in K562 cells, the human chronic myelogenous leukaemia cell line, are 40.1% and 9.3% of YT cells, respectively (Figure 2B, C). Therefore, what

we have observed in EN-NK/T-NT tissues and cell lines strongly imply the possibility that post-transcriptional regulation Compound C solubility dmso may abrogate the PRDM1 protein expression. Altered miRNA expression in EN-NK/T-NT lymphoma miRNAs are a novel class of non-coding small RNAs that negatively regulate protein expression via specific binding to their target sites in the 3′-UTR of their target mRNAs, initiating a translational blockade or the degradation of target mRNAs. We have previously confirmed the upregulation of

miR-223 and miR-886-3p and the downregulation of miR-34c-5p in EN-NK/T-NT cases; these changes are significantly different from those occurring in inflammatory nasal mucosa based on global miRNA expression profiling and qRT-PCR miRNA assays [21]. We hypothesised that in addition to the frequent deletions and DNA methylation reported previously, aberrant miRNAs may be responsible for the downregulation of the PRDM1 protein in EN-NK/T-NT. Because of the highly inflammatory background of EN-NK/T-NT, we used ISH to determine the expression status of miR-223, miR-886-3p, and miR-34c-5p in tumour cells. ISH analysis of FFPE tissues from EN-NK/T-NT demonstrated strong expression of miR-223 and miR-886-3p in the cytoplasm

of EN-NK/T-NT tumour cells and weak to no staining in peripheral T-cell lymphoma or inflammatory nasal mucosa; miR-34c-5p staining was weak in most samples from these 3 groups. Representative ISH results for miR-223, miR-886-3p, PR-171 ic50 and miR-34c-5p are shown in Figure 3. As shown in Figure 4A, the expression of miR-223 was statistically greater in EN-NK/T-NT cancer cells than in peripheral T-cell lymphoma (P = 0.013) and inflammatory nasal mucosa samples (P = 0.043). In addition, miR-886-3p also upregulated in EN-NK/T-NT samples, which was significantly different from peripheral T-cell lymphoma (P = 0.028) and inflammatory nasal mucosa samples (P = 0.022) (Figure 4B). Nevertheless, miR-34c-5p expression showed no significant difference between primary EN-NK/T-NT, peripheral T-cell lymphoma, and inflammatory nasal mucosa tissues (P = 1.000 and P = 0.254, respectively) (Figure 4C). In addition, the ISH results of miR-223, miR-886-3p, and miR-34c-5p were cross-validated with qRT-PCR results in 15 EN-NK/T-NT FFPE cases.