Abstract: ObjectiveTo investigate the expression of MKP3 in glioblastoma （GBM） and the effect of MKP3 overexpression on GBM cell proliferation and its possible molecular mechanism. 
MethodsTCGA database was used to analyze the expression of MKP3 in GBM and the survival of patients with different MKP3 expression. U87 MG cells was transfected with siMKP3 and siNC. The proliferation of glioblastoma U87 MG cell line was detected by MTT assay and EdU flow cytometry. Western blotting was used to detect the protein expression of pAKT， AKT， MKP3 and GAPDH. The role of PI3K／AKTMKP3 axis in the proliferation of glioblastoma was determined by a 1 μmol／L PI3K specific inhibitor and a pCDHMKP3 overexpression plasmid. 
ResultsThe analysis of TCGA database showed that the expression of MKP3 in GBM was significantly higher than that of normal tissue， and the difference was statistically significant （P＜005）； and the survival rate of patients with MKP3 high expression was significantly lower than that of patients with MKP3 low expression， and the difference was statistically significant （P＜005）. The MTT assay showed that the cell proliferation activity of the MKP3 expression silencing group was （0431±0116） significantly lower than that of the NC group （0986 ± 0056）， and the difference was statistically significant （P＜005）. The results of EdU showed that silencing MKP3 expression significantly inhibited the proliferation of U87 MG cells. Inhibition of PI3K／AKT signaling pathway can significantly block the proliferation of U87 MG cells. After overexpressed MKP3， the proliferation ability of U87 MG cells basically recovered. Overexpression of MKP3 did not increase the phosphorylation of AKT. 
ConclusionPI3K／AKT signaling pathway can promote the proliferation of GBM cells and increase the development of glioblastoma by up regulating MKP3 expression.

Key words: Glioblastoma（GBM）, MKP3, PI3K／AKT, Proliferation