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 aged between 23 and 42 years with a prevalence of 6%-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 Cell Counting Kit-8. Cell cycle/apoptosis was monitored using a flow cytometer. Cell invasion was studied by a Transwell assay. Quantitative RT-PCR and Western blot analyses were used to evaluate gene expression. S100A7 and NF-kappa B expression is increased in both endometriotic tissue and ESCs from women with EM. The expression of S100A7 is correlated with the expression of NF-kappa B. S100A7 knockdown inhibits ESCs proliferation, cell cycle progression, cell invasion, and inflammation, but promotes cell apoptosis in an NF-kappa B 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 the NF-kappa B dependent manner. These findings highlight the importance of S100A7/NF-kappa B signaling in EM and provide new insights into therapeutic strategies for EM.

Automated summary

The study found that the S100A7/NF-κB signaling pathway plays a crucial role in the pathogenesis of endometriosis, with S100A7 overexpression promoting the disease by increasing cell proliferation and inflammation, while decreasing cell apoptosis. This provides new insights into future therapeutic strategies.