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CD7 in acute myeloid leukemia: correlation with loss of wild-type CEBPA, consequence of epigenetic regulation
BACKGROUND: CD7 is a negative prognostic marker in myeloid malignancies. In acute myeloid leukemia (AML), an inverse correlation exists between expression of wild-type CEBPA and CD7. Aim of this study was to find out whether C/EBPα is a negative regulator of CD7 and which other regulatory mechanisms...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2873354/ https://www.ncbi.nlm.nih.gov/pubmed/20398252 http://dx.doi.org/10.1186/1756-8722-3-15 |
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author | Röhrs, Sonja Scherr, Michaela Romani, Julia Zaborski, Margarete Drexler, Hans G Quentmeier, Hilmar |
author_facet | Röhrs, Sonja Scherr, Michaela Romani, Julia Zaborski, Margarete Drexler, Hans G Quentmeier, Hilmar |
author_sort | Röhrs, Sonja |
collection | PubMed |
description | BACKGROUND: CD7 is a negative prognostic marker in myeloid malignancies. In acute myeloid leukemia (AML), an inverse correlation exists between expression of wild-type CEBPA and CD7. Aim of this study was to find out whether C/EBPα is a negative regulator of CD7 and which other regulatory mechanisms might be involved. RESULTS: As already described for primary AML cells, the majority of AML cell lines tested were either C/EBPα(+)/CD7(- )or C/EBPα(-)/CD7(+). However, the existence of isolated CD7(+ )cell lines expressing wild-type C/EBPα challenges the notion that C/EBPα acts as a unique repressor of CD7. Furthermore, ectopic expression of CEBPA did not reduce CD7 in CD7(+ )cells and knock-down of C/EBPα failed to induce CD7 in CD7(- )cells. In contrast, the DNA demethylating agent Aza-2'deoxycytidine triggered CD7 expression in CD7(- )AML and in T-cell lines suggesting epigenetic regulation of CD7. Bisulfite sequencing data confirmed that CpGs in the CD7 exon1 region are methylated in CD7(- )cell lines, and unmethylated in CD7(+ )cell lines. CONCLUSION: We confirmed an inverse correlation between the expression of wild-type CEBPA and of CD7 in AML cells. Our results contradict the hypothesis that C/EBPα acts as repressor for CD7, and instead show that epigenetic mechanisms are responsible for CD7 regulation, in AML cells as well as in T-cells, the typical CD7 expressing cell type. |
format | Text |
id | pubmed-2873354 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-28733542010-05-20 CD7 in acute myeloid leukemia: correlation with loss of wild-type CEBPA, consequence of epigenetic regulation Röhrs, Sonja Scherr, Michaela Romani, Julia Zaborski, Margarete Drexler, Hans G Quentmeier, Hilmar J Hematol Oncol Research BACKGROUND: CD7 is a negative prognostic marker in myeloid malignancies. In acute myeloid leukemia (AML), an inverse correlation exists between expression of wild-type CEBPA and CD7. Aim of this study was to find out whether C/EBPα is a negative regulator of CD7 and which other regulatory mechanisms might be involved. RESULTS: As already described for primary AML cells, the majority of AML cell lines tested were either C/EBPα(+)/CD7(- )or C/EBPα(-)/CD7(+). However, the existence of isolated CD7(+ )cell lines expressing wild-type C/EBPα challenges the notion that C/EBPα acts as a unique repressor of CD7. Furthermore, ectopic expression of CEBPA did not reduce CD7 in CD7(+ )cells and knock-down of C/EBPα failed to induce CD7 in CD7(- )cells. In contrast, the DNA demethylating agent Aza-2'deoxycytidine triggered CD7 expression in CD7(- )AML and in T-cell lines suggesting epigenetic regulation of CD7. Bisulfite sequencing data confirmed that CpGs in the CD7 exon1 region are methylated in CD7(- )cell lines, and unmethylated in CD7(+ )cell lines. CONCLUSION: We confirmed an inverse correlation between the expression of wild-type CEBPA and of CD7 in AML cells. Our results contradict the hypothesis that C/EBPα acts as repressor for CD7, and instead show that epigenetic mechanisms are responsible for CD7 regulation, in AML cells as well as in T-cells, the typical CD7 expressing cell type. BioMed Central 2010-04-14 /pmc/articles/PMC2873354/ /pubmed/20398252 http://dx.doi.org/10.1186/1756-8722-3-15 Text en Copyright ©2010 Röhrs et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Röhrs, Sonja Scherr, Michaela Romani, Julia Zaborski, Margarete Drexler, Hans G Quentmeier, Hilmar CD7 in acute myeloid leukemia: correlation with loss of wild-type CEBPA, consequence of epigenetic regulation |
title | CD7 in acute myeloid leukemia: correlation with loss of wild-type CEBPA, consequence of epigenetic regulation |
title_full | CD7 in acute myeloid leukemia: correlation with loss of wild-type CEBPA, consequence of epigenetic regulation |
title_fullStr | CD7 in acute myeloid leukemia: correlation with loss of wild-type CEBPA, consequence of epigenetic regulation |
title_full_unstemmed | CD7 in acute myeloid leukemia: correlation with loss of wild-type CEBPA, consequence of epigenetic regulation |
title_short | CD7 in acute myeloid leukemia: correlation with loss of wild-type CEBPA, consequence of epigenetic regulation |
title_sort | cd7 in acute myeloid leukemia: correlation with loss of wild-type cebpa, consequence of epigenetic regulation |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2873354/ https://www.ncbi.nlm.nih.gov/pubmed/20398252 http://dx.doi.org/10.1186/1756-8722-3-15 |
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