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PTPN3 in cancer: unveiling its immune-mediated impact on prognosis and dysregulated signaling pathways
Mostafa A Abdel-Maksoud1, Sajid Ullah2, Amun Nadeem3
1Department of Botany and Microbiology, College of Science, King Saud University P.O. Box 2455, Riyadh 11451, Saudi Arabia.
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.
Insights
Protein Tyrosine Phosphatase, Non-Receptor Type 3 (PTPN3) is upregulated across many cancers, particularly in breast cancer and lung adenocarcinoma. PTPN3 dysregulation impacts survival and the tumor immune microenvironment, offering prognostic and therapeutic potential.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Oncogenic processes involve critical gene dysregulation.
- Protein Tyrosine Phosphatase, Non-Receptor Type 3 (PTPN3) is implicated in various cellular functions.
- Understanding PTPN3's role in cancer is crucial for diagnostics and prognostics.
Purpose of the Study:
- To investigate the diagnostic and prognostic implications of PTPN3 in a pan-cancer context.
- To elucidate the role of PTPN3 in tumorigenesis, focusing on breast cancer (BRCA) and lung adenocarcinoma (LUAD).
- To explore PTPN3's impact on the tumor immune microenvironment and identify potential therapeutic targets.
Main Methods:
- Analysis of comprehensive genomic datasets.
- Experimental validation of PTPN3 expression and function.
- Mutational and promoter methylation analysis.
- Correlation analysis with immune cell infiltration and pathway enrichment.
- Drug prediction analysis.
Main Results:
- PTPN3 is ubiquitously upregulated across 33 cancer types.
- PTPN3 upregulation correlates with reduced overall survival in BRCA and LUAD.
- PTPN3 stability is observed in BRCA and LUAD, with hypomethylation driving dysregulation.
- PTPN3 expression positively correlates with CD8+ T cell infiltration.
- Potential therapeutic drugs targeting PTPN3 were identified.
Conclusions:
- PTPN3 is significantly upregulated in BRCA and LUAD, serving as a prognostic marker.
- Epigenetic regulation, specifically hypomethylation, plays a key role in PTPN3 dysregulation.
- PTPN3 influences the tumor immune microenvironment and presents therapeutic opportunities.
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