S100A1 overexpression stimulates cell proliferation and is predictive of poor outcome in ovarian cancer.

Background: Members of the S100 gene family are frequently dysregulated in various cancers, including ovarian cancer (OC). Despite this, the prognostic implications of individual S100 genes in OC remain poorly understood. This study aimed to explore the prognostic significance of S100A1 expression in OC and assess its potential as a therapeutic target.

Methods: To investigate the role of S100A1 in OC, we utilized the Gene Expression Profiling Interactive Analysis (GEPIA) database and the University of ALabama at Birmingham Cancer Data Analysis Portal (UALCAN) database. Protein levels of S100A1 in OC tissues were assessed using western blotting and immunohistochemistry. Bioinformatics analyses were performed to correlate S100A1 expression with clinical outcomes. Functional assays were conducted to evaluate the impact of S100A1 knockout on OC cell proliferation and migration. Additionally, we investigated the effect of S100A1 on ferroptosis and lipid reactive oxygen species (ROS) levels in tumor cells.

Results: Our analyses revealed that S100A1 protein levels were significantly elevated in OC tissues compared to normal tissues. Elevated S100A1 expression was associated with poor clinical outcomes in OC patients. Functional assays demonstrated that the knockout of S100A1 led to a decrease in both proliferation and migration of OC cells in vitro. Furthermore, S100A1 was found to inhibit ferroptosis in OC cells, resulting in lower levels of lipid ROS within tumor cells.

Conclusions: High levels of S100A1 are indicative of adverse clinical outcomes in OC. Our findings suggest that S100A1 could serve as a valuable prognostic marker and a potential therapeutic target for OC treatment.