Intersection analysis revealed three consistently dysregulated genes (PSMD4, PYCR2, and SEM1) across all comparison sets (LINC02878-overexpressing LoVo cells, TCGA tumor samples, stage groups, and survival cohorts), suggesting their potential as core downstream effectors of LINC02878-mediated oncogenesis (Fig. 3D, Figure S1). This evidence concerns the gene PYCR2 and neoplasm.