Phosphorylated-EGFR and MMP7 upregulation in gastric cancer: Association with metastasis and poor prognosis

Aggressive invasion and metastatic dissemination of gastric cancer (GC) are two major clinical challenges that frequently arise following standard treatments, markedly compromising patient outcomes. Elucidating the molecular drivers of GC progression would be key to developing effective therapeutic strategies. The present study employed an integrated approach combining bioinformatics analysis and immunohistochemical (IHC) validation to identify the key molecular players in GC metastasis. The Cancer Genome Atlas (TCGA) database analysis demonstrated marked upregulation of both epidermal growth factor receptor (EGFR) and matrix metalloproteinase 7 (MMP7) in gastric adenocarcinoma and elevated expression levels notably associated with poor patient prognosis. MMP7 expression exhibited a particularly robust association with metastatic progression, highlighting its potential role in facilitating tumor dissemination and experimental validation using IHC analysis of clinical specimens confirmed the coordinated involvement of both phosphorylated (p)-EGFR and MMP7 in metastatic processes. Notably, the present study identified a positive correlation between p-EGFR and MMP7 expression, suggesting a potential mechanistic interplay between these molecules in driving GC metastasis. These findings provide notable evidence that p-EGFR and MMP7 collectively contribute to GC progression and metastasis. The correlation between these markers offered novel insights into potential cooperative signaling pathways and presented a rational basis for the development of dual-targeted therapeutic approaches. The present study established a key foundation for future research aimed at disrupting the metastatic pathways in GC through targeted inhibition of p-EGFR and MMP7.