Selenoprotein GPX3 suppresses gastric adenocarcinoma proliferation and improves patient survival.

Stomach adenocarcinoma (STAD) is a highly prevalent and lethal malignancy worldwide, with its occurrence and progression regulated by multiple factors. In recent years, selenoprotein glutathione peroxidase 3 (GPX3) has gained significant attention due to its antioxidant properties and role in cellular oxidative stress regulation across various cancers. Our study delved into the expression of GPX3 in STAD and investigated its impact on tumor cell growth, providing insights into its potential anti-tumor mechanisms. The expression levels of GPX3 were analyzed in STAD tissues sourced from the TCGA database and contrasted with the levels found in normal gastric tissues. The expression levels of GPX3 were contrasted between STAD tissues and normal gastric tissues, and their correlation with patient prognosis was assessed by survival analysis. Additionally, we validated GPX3 expression changes and its effects on tumor cell growth using quantitative PCR (qPCR) and CCK-8 proliferation assays in STAD cell lines (MNK-45, MGC-803, N87, and HGC-27). Our findings suggest that GPX3 expression is significantly downregulated in STAD tissues compared to normal gastric tissues. Survival analysis further reveals that patients with high GPX3 expression exhibit better long-term survival rates, suggesting a potential tumor-suppressive function. In vitro experiments confirmed effective knockdown or overexpression of GPX3 in STAD cell lines. CCK-8 proliferation assays demonstrated that GPX3 overexpression significantly inhibited tumor cell proliferation, whereas GPX3 knockdown promoted cell growth. This study provides new experimental evidence supporting GPX3 as a potential therapeutic target for STAD and offers a theoretical foundation for future molecular-targeted therapies for STAD.