PTPRC as a pan-cancer biomarker: Prognostic significance and immune microenvironment interactions

This study investigated the role of Protein Tyrosine Phosphatase Receptor type C (PTPRC) in various cancers using bioinformatics analyses and experimental validation. We analyzed public databases (TIMER2.0, GEPIA2, cBioPortal) and single-cell sequencing data to evaluate PTPRC expression differences, patient prognosis, and immune microenvironment associations in tumors. RT-qPCR was employed to validated PTPRC expression in nasopharyngeal carcinoma (CNE2) and hepatocellular carcinoma (HePG2) cell lines. Our findings revealed that PTPRC was upregulated in 11 tumor types (P < 0.05) and associated with worse survival in 6 cancers (P < 0.05). It was correlated with immune cell infiltration, immune checkpoint genes (ICGs), cancer-associated fibroblasts (CAFs), tumor mutation burden (TMB), and microsatellite instability (MSI) (P < 0.05). Single-cell analysis indicated PTPRC is closely related to angiogenesis, differentiation, proliferation, and quiescence in certain tumors. Functional enrichment analysis emphasized PTPRC's involvement in T-cell receptor (TCR) and PD-L1/PD-1 signaling pathways, highlighting its role in T-cell activation, immune tolerance, and tumor progression. Experimental validation confirmed that PTPRC was upregulated in CNE2 cells compared to normal nasopharyngeal epithelial cells and downregulated in HePG2 cells compared to normal hepatocytes, consistent with bioinformatics results. In conclusion, abnormal PTPRC expression in pan-cancer may drive tumor development through multiple mechanisms, indicating its potential as a therapeutic target, especially in immunotherapy.