Complexity of miR-223 regulation by CEBPA in human AML

被引：50

作者：

Eyholzer, Marianne ^{[1
]}

Schmid, Sabine ^{[1
]}

Schardt, Julian A. ^{[1
]}

Haefliger, Simon ^{[1
]}

Mueller, Beatrice U. ^{[2
]}

Pabst, Thomas ^{[1
]}

机构：

[1] Univ Bern, Inselspital, Univ Hosp Bern, Inst Med Oncol, CH-3010 Bern, Switzerland

[2] Univ Bern, Inselspital, Univ Hosp Bern, Dept Internal Med, CH-3010 Bern, Switzerland

来源：

LEUKEMIA RESEARCH | 2010年 / 34卷 / 05期

基金：

瑞士国家科学基金会;

关键词：

AML; CEBPA; miR-223; NFIA; PU.1; Transcriptional regulation; ACUTE MYELOID-LEUKEMIA; MICRORNA EXPRESSION; C/EBP-ALPHA; DIFFERENTIATION;

D O I：

10.1016/j.leukres.2009.11.019

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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. (C) 2009 Elsevier Ltd. All rights reserved.

引用

页码：672 / 676

页数：5

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