MiR-24 improves beta-like globin gene expression through targeting Sp1.
- Author:
Yanni MA
1
;
Bin WANG
;
Bei GONG
;
Fang WANG
;
Hualu ZHAO
;
Junwu ZHANG
;
Jia YU
Author Information
1. State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences (CAMS) & Peking Union Medical College (PUMC), Beijing 100005, China.
- Publication Type:Journal Article
- MeSH:
Cell Differentiation;
Gene Expression Regulation;
Hematopoietic Stem Cells;
metabolism;
Humans;
K562 Cells;
MicroRNAs;
genetics;
Sp1 Transcription Factor;
genetics;
epsilon-Globins;
genetics;
gamma-Globins;
genetics
- From:
Chinese Journal of Biotechnology
2013;29(7):946-954
- CountryChina
- Language:Chinese
-
Abstract:
We studied the function and mechanism of miR-24 in regulating beta-like globin gene expression. We first detected the expression of miR-24 during erythroid differentiation and also detected the globin gene expression in miR-24 overexpressing K562 cells through q-PCR. Dual-luciferase reporter assay and Western blotting were used to identify target genes of miR-24. "Rescue experiment" was further used to investigate the regulation of miR-24 on globin gene expression whether depending on targeting Sp1 or not. We found that miR-24 increased during hemin-induced K562 cells and EPO-induced HPCs (hematopoietic progenitor cells) erythroid differentiation. Overexpression of miR-24 in K562 cells promoted the epsilon- and gamma-globin gene expression during hemin-induced erythroid differentiation through targeting the negative globin regulator Sp1. These results suggested that miR-24 can improve the expression of beta-like globin gene through targeting Sp1.
