Complexity of miR-223 regulation by CEBPA in human AML

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

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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 and Pabst, Thomas

ISSN:

0145-2126

Publisher:

Elsevier

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:07

Last Modified:

04 May 2014 23:04

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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