Endogenous FOXP3 inhibits cell proliferation, migration and invasion in glioma cells.

The transcription factor forkhead box P3 (FOXP3) has been demonstrated to play important roles in the development and function of regulatory T cells (Tregs). In addition, studies had recently demonstrated that FOXP3 also expressed in some tumor cells. However, the exact role and molecular mechanism of FOXP3 function in glioma's cells are still unclear. This study aims to elucidate the functions of FOXP3 in glioma's cells. Expression of FOXP3 in glioma cell U87 and LN229 was up-regulated and down-regulated by pCMV6-FOXP3-GFP and pRFP-C-RS shFOXP3 respectively. Then, CCK-8 assay, flow cytometry, migration and invasion assay, and western blot were used to detect cell proliferation, cell cycle, cell migration and invasion and related protein expression. All detection methods demonstrated that over-expression of FOXP3 in glioma cell U87 and LN229 inhibited cell proliferation, reduced cell migration, decreased cell invasion compared with control. Moreover, up-regulation of FOXP3 increased the protein levels of pro-apoptotic molecules caspases-3 and caspases-7, resulting in the promotion of cell apoptosis. Conversely down-regulation of the FOXP3 promoted cell growth and inhibited cell apoptosis and reduced the expression of caspases-3 and caspases-7. Our findings suggest that FOXP3 maybe act as a suppressor in glioma cells proliferation, migration and invasion and endogenous FOXP3 transfusion could be a novel approach for inhibiting glioma progression.