PTPN3 in cancer: unveiling its immune-mediated impact on prognosis and dysregulated signaling pathways.

Objectives: Oncogenic processes in cancer are frequently marked by the dysregulation of critical genes, and PTPN3 (Protein Tyrosine Phosphatase, Non-Receptor Type 3) has emerged as a gene of interest due to its potential involvement in various cellular processes. This study delves into the diagnostic and prognostic implications of PTPN3 in a pan-cancer context.

Methods: Leveraging comprehensive genomic datasets and experimental validation, we aimed to shed light on the role of PTPN3 in cancer.

Results: Our findings revealed the pervasive up-regulation of PTPN3 across 33 cancer types, making it a ubiquitous player in tumorigenesis. Of particular note, PTPN3 up-regulation exhibited a strong association with reduced overall survival in breast cancer (BRCA) and lung adenocarcinoma (LUAD). This underscores PTPN3's potential as a valuable prognostic marker in these cancers. While genetic mutations often drive oncogenic processes, our mutational analysis demonstrated the relative stability of PTPN3 in BRCA and LUAD. Promoter methylation analysis showed that hypomethylation plays a predominant role in PTPN3 dysregulation in BRCA and LUAD. Furthermore, our study unveiled positive correlations between PTPN3 expression and CD8+ T cell infiltration, offering insights into the gene's influence on the tumor immune microenvironment. Pathway enrichment analysis highlighted the involvement of PTPN3-associated genes in crucial signaling pathways. In addition, drug prediction analysis pinpointed potential drugs capable of modulating PTPN3 expression, opening avenues for personalized treatment strategies.

Conclusion: In summary, our study elucidates the multifaceted roles of PTPN3 in BRCA and LUAD, underlining its significant up-regulation, prognostic relevance, epigenetic regulation, and its impact on the tumor immune microenvironment.