Open AccessMicroRNA‐223 reversibly regulates erythroid and megakaryocytic differentiation of K562 cells
Author(s) -
Yuan JinYun,
Wang Fang,
Yu Jia,
Yang GuiHua,
Liu XiaoLing,
Zhang JunWu
Publication year - 2009
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2008.00585.x
Subject(s) - k562 cells , microrna , microbiology and biotechnology , cellular differentiation , chemistry , granulopoiesis , erythropoiesis , biology , 3t3 cells , transfection , haematopoiesis , cell culture , leukemia , stem cell , immunology , biochemistry , medicine , gene , anemia , genetics
MicroRNAs (miRNAs) are thought to modulate a variety of cellular events. Several studies have revealed the functions of miR‐223 in granulopoiesis. Here we analysed miR‐223 expression in various human tissues, blood and leukaemia cells, and focused on its role in K562 erythroid and megakaryocytic differentiation. MiR‐223 was detected not only in granulocytes but also in erythroid cells. In K562 cells, expression of miR‐223 was down‐regulated during haemin‐induced erythroid differentiation but up‐regulated during phorbol myristate acetate (PMA)‐induced megakaryocytic differentiation. The overexpression of miR‐223 resulted in significant decrease of γ‐globin mRNA and the fraction of benzidine‐positive cells in K562 cells, suggesting a suppressive effect of miR‐223 on erythroid differentiation. Peaks corresponding to 4N cells in stable transfectants overexpressing miR‐223 were higher than that in control K562 cells during megakaryocytic differentiation, indicating that miR‐223 increases megakaryocytic differentiation. The expression of LIM domain only 2 (LMO2) reporter was suppressed in NIH‐3T3 when the expression of miR‐223 was enforced by both the luciferase and fluorescence system. Furthermore, LMO2 mRNA and protein levels were significantly decreased in stable K562 transfectants overexpressing miR‐223. These results indicate that LMO2 is a direct target of miR‐223. Thus, our results suggest that miR‐223 reversibly regulates erythroid and megakaryocytic differentiation of K562 cells via down‐modulation of LMO2.