Journal
FEBS LETTERS
Volume 586, Issue 7, Pages 1038-1043Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2012.02.050
Keywords
FOXO1; MicroRNA-223; Cell proliferation
Funding
- National Natural Science Foundation of China [30570414, 30970641, 31170767]
- State Key Laboratory of Medical Neurobiology, Fudan University
- National Key Basic Research Program of China [2012CB822104]
- Hi-Tech Research Development Program of Wenzhou [H20100018]
- Shanghai Leading Academic Discipline Project [B110]
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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. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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