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Abstract
The transcription factor Forkhead Box P3 (Foxp3) has been shown to play important
roles in the occurring of regulatory T cells (Tregs). Limited evidence indicated that
it was also expressed in tissues other than thymus and spleen, while, very recently,
it was identified as a suppressor gene in breast cancer. However, the precise role
and molecular mechanism of the action of Foxp3 in ovarian cancer remained unclear.
To elucidate the function of Foxp3, we examined the expression of Foxp3 in ovarian
cancerous cells and the consequences of up-regulation of Foxp3 in epithelial ovarian
cancer cell lines, respectively. By multiple cellular and molecular approaches such
as gene transfection, CCK-8 assay, flow cytometry, RT-PCR, in-cell western, wound
healing assay, and invasion assay, we found that Foxp3 was weakly/no expressed in
ovarian cancerous cells. Up-regulation of Foxp3 inhibited cell proliferation, decreased
cell migration, and reduced cell invasion. Compared with control, Foxp3 up-regulated
cells showed decreased expression of Ki-67 and cyclin-dependent kinases (CDKs). Moreover,
up-regulation of Foxp3 reduced the expression of matrix metalloproteinase-2 (MMP-2)
and urokinase-type plasminogen activator (uPA), resulting in the inhibition of cell
migration and invasion. In addition, Foxp3 up-regulation inhibited the activation
of mammalian target of rapamycin (mTOR) and NF-kappaB signaling. These findings suggested
that up-regulation of Foxp3 could be a novel approach for inhibiting ovarian cancer
progression.
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