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Over‐expression of EDAG in the myeloid cell line 32D: Induction of GATA‐1 expression and erythroid/megakaryocytic phenotype
Author(s) -
Ding Yali,
Xu ChengWang,
Wang ZhiDong,
Zhan YiQun,
Li Wei,
Xu WangXiang,
Yu Miao,
Ge ChangHui,
Li ChangYan,
Yang XiaoMing
Publication year - 2010
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22597
Subject(s) - biology , transcription factor , haematopoiesis , gene , phenotype , gene silencing , gata1 , rna interference , myeloid , microbiology and biotechnology , gene expression , cell culture , genetics , rna , cancer research , stem cell
Erythroid differentiation‐associated gene (EDAG), a hematopoietic tissue‐specific transcription regulator, plays a key role in maintaining the homeostasis of hematopoietic lineage commitment. However, the mechanism and genes regulated by EDAG remain unknown. In this study, we showed that overexpression of EDAG in a myeloid cell line 32D led to an erythroid phenotype with increased number of benzidine‐positive cells and up‐regulation of erythroid specific surface marker TER119. The megakaryocytic specific marker CD61 was also induced significantly. Using a genome‐wide microarray analysis and a twofold change cutoff, we identified 332 genes with reduced expression and 288 genes with increased expression. Among up‐regulation genes, transcription factor GATA‐1 and its target genes including EKLF, NF‐E2, Gfi‐1b, hemogen, SCL, hemoglobin alpha, beta and megakaryocytic gene GPIX were increased. Silencing of EDAG by RNA interference in K562 cells resulted in down‐regulation of these genes. Taken together, EDAG functions as a positive regulator of erythroid/megakaryocytic differentiation in 32D cells associated with the induction of GATA‐1 and its target genes. J. Cell. Biochem. 110: 866–874, 2010. © 2010 Wiley‐Liss, Inc.