| Summary: | <p>Abstract</p> <p>Background</p> <p>CD7 is a negative prognostic marker in myeloid malignancies. In acute myeloid leukemia (AML), an inverse correlation exists between expression of wild-type <it>CEBPA </it>and <it>CD7</it>. Aim of this study was to find out whether C/EBPα is a negative regulator of <it>CD7 </it>and which other regulatory mechanisms might be involved.</p> <p>Results</p> <p>As already described for primary AML cells, the majority of AML cell lines tested were either C/EBPα<sup>+</sup>/CD7<sup>- </sup>or C/EBPα<sup>-</sup>/CD7<sup>+</sup>. However, the existence of isolated CD7<sup>+ </sup>cell lines expressing wild-type C/EBPα challenges the notion that C/EBPα acts as a unique repressor of <it>CD7</it>. Furthermore, ectopic expression of <it>CEBPA </it>did not reduce <it>CD7 </it>in CD7<sup>+ </sup>cells and knock-down of C/EBPα failed to induce <it>CD7 </it>in CD7<sup>- </sup>cells. In contrast, the DNA demethylating agent Aza-2'deoxycytidine triggered <it>CD7 </it>expression in CD7<sup>- </sup>AML and in T-cell lines suggesting epigenetic regulation of <it>CD7</it>. Bisulfite sequencing data confirmed that CpGs in the <it>CD7 </it>exon1 region are methylated in CD7<sup>- </sup>cell lines, and unmethylated in CD7<sup>+ </sup>cell lines.</p> <p>Conclusion</p> <p>We confirmed an inverse correlation between the expression of wild-type <it>CEBPA </it>and of <it>CD7 </it>in AML cells. Our results contradict the hypothesis that C/EBPα acts as repressor for <it>CD7</it>, and instead show that epigenetic mechanisms are responsible for <it>CD7 </it>regulation, in AML cells as well as in T-cells, the typical CD7 expressing cell type.</p>
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