The Effect and the Mechanism of miR-209 Targeted Regulating PI3K (Phosphatidylinositol3-Kinase)/AKT (Protein Kinase B)/FOXO3a (Forkhead box O3) Signaling Pathway on Glioma Stem Cells

Author:

Yuan Wen1,Zheng Wei1,Liu Chao1

Affiliation:

1. Department of Neurosurgery, Central Hospital of Zhuzhou, Zhuzhou, Hunan Province 412000, PR China

Abstract

To explore the role and mechanism of miR-209 target regulating PI3K/Akt/FOXO3a in glioma. GSCs were isolated from the lesions of glioma patients, cultured, passaged and characterized. Set blank control group (with saline solution), miR-209-mimics group (cells transfected with miR-209-mimics) and negative control group (cells transfected with meaningless sequences). After cell transfection, observe the transfection efficiency of miR-209 MIC, detect the miR-209 mRNA expression level and biological peptide ions such as proliferation, migration, invasion, and withering, and detect the expression of PI3K/Akt/FOXO3a-related proteins (PI3K, p-Akt, FOXO3a). The miR-209mRNA expression level in the miR-209 mimics group was much higher (P < 0.01), and they two had indifferent differentiation (P >0.05); 24, 48 and 72 hours after transfection, the cell migration, proliferation rate and invasion ability of the miR-209 mimics group were much stronger (P <0.05) and the cell apoptosis rate at 24, 48, and 72 hours after transfection was much less (P < 0.01) and they two had no scientific differences (P > 0.05). The PI3K and p-Akt protein expression in the glioma stem elements of the miR-209 transfected group was much higher (P <0.01). The expression of FOXO3a was much less (P <0.01), while the standard level of PI3K, P-Akt and FOXO3a protein had no obvious difference (P >0.05). miR-209 can activate PI3K/Akt/FOXO3a to promote the growth, reproduction and invasion of GSCs, and control the cells withering system. This will provide new avenues for clinical trials.

Publisher

American Scientific Publishers

Subject

Biomedical Engineering,Medicine (miscellaneous),Bioengineering,Biotechnology

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