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MicroRNA‐223 regulates FOXO1 expression and cell proliferation
Author(s) -
Wu Lihui,
Li Huihui,
Jia Cheng You,
Cheng Wei,
Yu Mei,
Peng Min,
Zhu Yuanqing,
Zhao Qianlei,
Dong Yi Wei,
Shao Kang,
Wu Anle,
Wu Xing Zhong
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.02.050
Subject(s) - foxo1 , microrna , cell growth , microbiology and biotechnology , expression (computer science) , chemistry , biology , signal transduction , computer science , biochemistry , gene , protein kinase b , programming language
In HCT116 colorectal cancer cells, HeLa cervical cancer cells and HuH‐7 hepatoma cells, miR‐223 is expressed at a low level. Through infection with lentivirus containing miR‐223 precursor, miR‐233 was overexpressed in all these cells. Interestingly, the expression levels of FOXO1 mRNA and protein, and phosphorylation levels became significantly lower than those of their control. FOXO1 was down‐regulated mainly in the cytoplasm, while the nuclear FOXO1 level became relatively high compared to the cytoplasm. As the unphosphorylated active form of FOXO1 increased in the cells, cyclin D1/p21/p27 were up‐regulated at either mRNA or protein level. Proliferation of the cells was also greatly inhibited when miR‐223 was over‐expressed. Therein, our data suggest that miR‐223 regulates FOXO1 expression and cell proliferation.