Abstract
Bladder cancer (BLCA) is a common malignancy of the urinary system, yet the therapeutic relevance of transient receptor potential cation channel subfamily M member 4 (TRPM4) remains unclear. By integrating single-cell and whole-genome transcriptomic data, this study revealed significant transient receptor potential cation channel subfamily M member 4 (TRPM4) overexpression in bladder cancer (BLCA) (p < 0.05), particularly in epithelial cells. Intersection analysis identified 220 candidate genes (7,808 DEGs1, 4,683 DEGs2, and 4,802 key cell module genes). A risk model was constructed comprising six screened prognostic marker genes, namely, protein unc-93 homolog B1 (UNC93B1), family with sequence similarity 193 member B (FAM193B), protein O-glucosyltransferase (POGLUT3), fibrillin-1 (FBN1), microtubule-associated protein 1B (MAP1B), and RUNX family transcription factor 2 (RUNX2). The model demonstrated marked differences among the risk groups. Gene set enrichment analysis revealed significant disparities in key pathways, including the melanoma pathway (p < 0.05). Furthermore, immune infiltration analysis has identified 12 distinct immune cell types, including naive B cells, which showed a p < 0.05 distribution. The observed distribution was uneven. In the drug sensitivity analysis, 112 drugs (including WZ3105; p < 0.05) showed differential responses, and UNC93B1 showed high positive expression in BLCA tissues (positive cell proportion > 75%). Our studies confirmed that TRPM4 has significant prognostic value and is a potential novel diagnostic and therapeutic target for BLCA.