RUNX1-Driven CPXM1 Transcription Promotes Malignant Phenotypes and EMT in Gastric Cancer Cells

Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, with current treatment strategies largely limited to surgery, chemotherapy, and targeted therapy. Although the glycoprotein CPXM1 has been implicated in tumorigenesis, its functional role and underlying molecular mechanisms in GC remain unclear. In this study, we demonstrated that CPXM1 is significantly upregulated in GC tissues, and that elevated CPXM1 expression is associated with an unfavorable prognosis in GC patients. Both in vitro and in vivo functional assays revealed that CPXM1 significantly promotes GC cell proliferation, invasion, and metastasis. Mechanistically, CPXM1 was found to facilitate epithelial-mesenchymal transition (EMT), a critical process driving cancer progression. Furthermore, we identified the transcription factor RUNX1 as a direct upstream regulator of CPXM1, which binds to the CPXM1 promoter and transcriptionally activates its expression. Collectively, these findings delineate a previously unrecognized RUNX1/CPXM1/EMT axis that contributes to GC malignant progression, highlighting CPXM1 as a potential diagnostic biomarker and therapeutic target.