S100A7 promotes the development of human endometriosis by activating NF-κB signaling pathway in endometrial stromal cells.

Endometriosis (EM) is a chronic inflammatory disease affecting women between ages of 23-42 years with a prevalence of 6% to 10%. S100A7, a member of the S100 protein family, has been implicated in promoting inflammation. However, the role of S100A7 in EM and its underlying mechanism remain to be elucidated. S100A7 was silenced or overexpressed in primary endometrial stromal cells (ESCs). Cell proliferation was determined using a CCK-8 kit. Cell cycle/apoptosis were monitored using a flow cytometer. Cell invasion was studied by a Transwell assay. Quantitative RT-PCR and western blots were used to evaluate gene expression. S100A7 and NF-κB expression is increased in both endometriotic tissue and ESCs from women with EM. Expression of S100A7 is correlated with the expression of NF-κB. S100A7 knockdown inhibits ESCs proliferation, cell cycle progression, cell invasion, and inflammation, but promotes cell apoptosis in a NF-κB dependent manner. In contrast, S100A7 overexpression demonstrated an inverse effect. S100A7 is increased in both endometriotic tissue and ESCs from women with EM. S100A7 overexpression contributes to EM through increasing ESCs proliferation, cell cycle progression, cell invasion, and inflammation, and inhibiting cell apoptosis in a NF-κB dependent manner. These findings highlight the importance of S100A7/NF-κB signaling in EM and provide new insights into therapeutic strategies for EM. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.