Published online Jun 15, 2025. doi: 10.4251/wjgo.v17.i6.105213
Revised: April 19, 2025
Accepted: May 13, 2025
Published online: June 15, 2025
Processing time: 150 Days and 5.6 Hours
Gastric cancer (GC) is a leading cause of cancer-related death worldwide. Hypo
To assess the relationship between EPAS1 expression and prognosis in GC and investigate its possible role in the development of GC.
EPAS1 expression in GC and adjacent tissues was assessed using immunohistochemistry. Correlations with clinicopathological features were analyzed by using The Cancer Genome Atlas (TCGA) and clinical data to evaluate its prognostic value. The TIMER2.0 database was used to examine associations between EPAS1 and immune-infiltrating cells. Gene set enrichment analysis identified the mecha
EPAS1 expression was significantly greater in GC tissues than in adjacent tissues (P < 0.05). High EPAS1 expression was correlated with shorter overall survival (OS) and was associated with greater infiltration depth and poorer tumor differentiation (P < 0.05). Univariate and multivariate Cox analyses revealed that EPAS1 expression (HR: 2.095; 95%CI: 1.019-4.307; P < 0.001) was an independent predictor of OS. EPAS1 was enriched in the epithelial-mesenchymal transition (EMT), inflammatory response, KRAS, TGF-β, TNF-/NF-kB, and IL6/JAK/STAT3 signaling pathways. The high EPAS1 expression group presented increased levels of pathway-related molecules and immunotherapy checkpoints. In vitro and in vivo studies confirmed that silencing EPAS1 reduced GC cell invasion and metastasis.
EPAS1 may be a prognostic marker in patients with GC and may promote tumor growth through the immune response and pathways associated with EMT, inflammatory response, KRAS, TGF-β, TNF-/NF-kB,
Core Tip: EPAS1 expression is significantly higher in gastric cancer (GC) tissues than in adjacent tissues and is correlated with poor overall survival in patients with GC. High EPAS1 expression is associated with increased infiltration, poor tumor differentiation, and the activation of multiple signaling pathways, including the epithelial-mesenchymal transition, inflammatory response, KRAS, TGF-β, TNF-/NF-kB, and IL6/JAK/STAT3 pathways. EPAS1 also enhances the invasion and metastasis of GC cells. These findings suggest that EPAS1 may serve as an independent prognostic marker and contribute to tumor progression through immune responses and key signaling pathways.