Comprehensive pan‑cancer analysis of the glycolysis‑related gene STC1 and its role in gastric cancer

Cancer remains one of the leading causes of death globally. The enhanced glycolytic activity of tumor cells drives malignant progression, making glycolysis inhibition a promising therapeutic strategy. The glycolysis-associated gene stanniocalcin 1 (STC1) has been shown to influence glycolytic capacity and promote tumor growth in several cancers, yet its role remains poorly understood. In particular, whether STC1 regulates glycolytic capacity in gastric cancer (GC) has not been explored. In this study, we investigated the role of STC1 across cancer types using multiple online databases. We analyzed STC1 expression patterns and their associations with patient survival and prognosis. We further examined the immunological role of STC1 by correlating its expression with immune checkpoints, tumor stemness, immunomodulators, and immune cell infiltration. Additionally, we used small interfering RNA (siRNA) to assess the effects of STC1 on glycolysis and malignant progression in GC cells. Our analysis revealed that STC1 is highly expressed across multiple tumor types and that this elevated expression correlates with poor prognosis. In addition, STC1 expression was positively associated with immune cell infiltration, suggesting a potential role in remodeling the tumor microenvironment (TME). In GC, high STC1 expression was also linked to reduced survival. Knockdown of STC1 in GC cells reduced PI3K/Akt phosphorylation, downregulated the glycolytic enzymes HK2 and LDHA, decreased glycolytic capacity, and inhibited proliferation, invasion, and migration. These findings suggest that STC1 may regulate glycolysis in GC and could serve as both a prognostic biomarker and a therapeutic target, acting through its involvement in glucose metabolism and immune modulation. Targeting STC1 to suppress glycolysis may therefore represent a novel approach for GC therapy.