XXXX inhibits nuclear factor-kB pathway activation, and regulates adhesion, migration, invasion and apoptosis of endometriotic stromal cells.

@entity9135 @entity1476 @entity1356 @entity13373 @entity1759 @entity21055 @entity46 @entity1495 @entity14568
The activation of nuclear factor-kB (NF-kB) has been implicated in the development and progression of @entity46 . The aim of this study is to investigate the potential application of @entity13373 ( @entity14568 ), a potent NF-kB inhibitor, in the treatment of @entity46 . NF-kB-DNA-binding activity, IkB phosphorylation and expression of nuclear @entity9135 protein in endometriotic ectopic stromal cells (EcSCs), endometriotic eutopic stromal cells (EuSCs) and normal endometrial stromal cells (NESCs) were detected by electrophoretic mobility shift assay and western blot analysis. Adhesion, migration, invasion and apoptosis of EcSCs were observed by means of adhesion, migration, invasion and terminal deoxynucleotidyl transferase-mediated @entity21055 nick-end labeling assay, respectively. Gene and protein expressions of @entity1759 s, @entity1476 , @entity1495 and survivin in EcSCs were measured by RT-PCR and western blot analysis. The results showed that @entity14568 in the absence or presence of @entity1356 showed stronger inhibitory effects on NF-kB-DNA-binding activity, IkB phosphorylation and expression of nuclear @entity9135 protein in EcSCs than those in EuSCs or NESCs. @entity14568 enhanced apoptosis, and suppressed @entity1356 -induced cellular adhesion, migration and invasion of EcSCs. Pretreatment of EcSCs with @entity14568 attenuated @entity1356 -induced expressions of CD44s, @entity1476 , @entity1495 and survivin at gene and protein levels. All these findings suggest that @entity14568 induces apoptosis and down-regulates adhesion, migration and invasion of EcSCs through the suppression of various molecules. Therefore, @entity14568 could be used as a therapeutic agent for the treatment of @entity46 .
