Eyholzer, Marianne; Schmid, Sabine; Schardt, Julian A; Haefliger, Simon; Mueller, Beatrice U; Pabst, Thomas (2010). Complexity of miR-223 regulation by CEBPA in human AML. Leukemia research, 34(5), pp. 672-6. Amsterdam: Elsevier 10.1016/j.leukres.2009.11.019
Full text not available from this repository. (Request a copy)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.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Department of General Internal Medicine (DAIM) > Clinic of General Internal Medicine > Centre of Competence for General Internal Medicine 04 Faculty of Medicine > Department of Haematology, Oncology, Infectious Diseases, Laboratory Medicine and Hospital Pharmacy (DOLS) > Clinic of Medical Oncology |
UniBE Contributor: |
Müller, Beatrice Ursula, Pabst, Thomas Niklaus |
ISSN: |
0145-2126 |
Publisher: |
Elsevier |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 14:07 |
Last Modified: |
02 Mar 2023 23:20 |
Publisher DOI: |
10.1016/j.leukres.2009.11.019 |
PubMed ID: |
20018373 |
Web of Science ID: |
000276945300020 |
URI: |
https://boris.unibe.ch/id/eprint/100 (FactScience: 195877) |
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