Leukemia research, 2010-05, Vol.34 (5), p.672-676
2010
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- Autor(en) / Beteiligte
- Titel
- Complexity of miR-223 regulation by CEBPA in human AML
- Ist Teil von
- Leukemia research, 2010-05, Vol.34 (5), p.672-676
- Ort / Verlag
- England: Elsevier Ltd
- Erscheinungsjahr
- 2010
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Abstract microRNA-223 (miR-223) can trigger normal granulopoiesis. miR-223 expression is regulated by two distinct CEBPA (CCAAT/enhancer binding protein-alpha) sites. Here, we report that miR-223 is largely suppressed in cells from acute myeloid leukemia (AML) patients. By sequencing, we found that miR-223 suppression in AML is not caused by DNA sequence alterations, nor is it mediated by promoter hypermethylation. The analysis of the individual contribution of both CEBPA sites to miR-223 regulation identified the site upstream of the miR-223 primary transcript as the predominant regulatory element. Our results suggest that miR-223 suppression in AML is caused by impaired miR-223 upstream factors.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0145-2126eISSN: 1873-5835DOI: 10.1016/j.leukres.2009.11.019Titel-ID: cdi_proquest_miscellaneous_744615898
- Format
- –
- Schlagworte
- AML, Base Sequence, Blotting, Western, CCAAT-Enhancer-Binding Proteins - genetics, CEBPA, Electrophoretic Mobility Shift Assay, Gene Expression, Gene Expression Regulation, Leukemic - genetics, Hematology, Oncology and Palliative Medicine, Humans, Leukemia, Myeloid, Acute - genetics, MicroRNAs - genetics, miR-223, Molecular Sequence Data, NFIA, Polymorphism, Single Nucleotide, Promoter Regions, Genetic, PU.1, Reverse Transcriptase Polymerase Chain Reaction, Transcriptional regulation