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Published on: February 8, 2018
Low CTDNEP1 Expression Predicts Poor Prognosis and Is Associated With Immune Modulation in Pancreatic Cancer
Mayuka Nii1, Tadayoshi Hayata2
1Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences and Faculty of Pharmaceutical Science, Tokyo University of Science, Tokyo, Japan.
Background/Aim:
Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal malignancy due to limited therapeutic options. Identifying novel genes that influence its progression is critical. This study aimed to investigate the role of CTDNEP1, a phosphatase-encoding gene, in PDAC using multi-omics data from The Cancer Genome Atlas (TCGA).
Materials And Methods:
We analyzed CTDNEP1 expression in PDAC using the TCGA and Pan-Cancer Atlas datasets. Kaplan-Meier survival analysis was performed to assess the association between CTDNEP1 expression and patient prognosis. Gene Ontology (GO) and KEGG pathway enrichment analyses were conducted to explore the biological processes linked to CTDNEP1 expression. Finally, we examined the relationship between CTDNEP1 expression and the tumor immune microenvironment using immune infiltration analysis.
Results:
CTDNEP1 expression was found to be significantly lower in PDAC tissues compared to normal tissues, especially in early-stage tumors. This downregulation was associated with mutations in key driver genes, including KRAS, CDKN2A, TP53, and SMAD4. Importantly, low CTDNEP1 expression correlated with significantly poorer patient prognosis, particularly in stage II PDAC. Functional enrichment analysis revealed that low CTDNEP1 expression is associated with macroautophagy, protein degradation, and immune/inflammatory pathways, while high expression is linked to mitochondrial function and metabolic activity. Furthermore, CTDNEP1 expression showed a positive correlation with immune cell infiltration.
Conclusion:
CTDNEP1 functions as a tumor suppressor in PDAC, influencing tumor progression, immune response, and patient survival. Future studies should investigate the detailed regulatory mechanisms of CTDNEP1 and explore its potential as a therapeutic target or biomarker for PDAC.
Insights
CTDNEP1 is downregulated in pancreatic cancer, correlating with poor prognosis and altered immune responses. This phosphatase may act as a tumor suppressor, offering potential therapeutic avenues.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy with limited treatment options.
- Identifying novel genes impacting PDAC progression is crucial for developing new therapies.
- CTDNEP1, a phosphatase-encoding gene, is investigated for its role in PDAC.
Purpose of the Study:
- To investigate the role of CTDNEP1 in pancreatic ductal adenocarcinoma (PDAC).
- To analyze CTDNEP1 expression patterns and their correlation with patient prognosis and tumor characteristics using multi-omics data.
Main Methods:
- Analyzed CTDNEP1 expression in PDAC using The Cancer Genome Atlas (TCGA) and Pan-Cancer Atlas datasets.
- Performed Kaplan-Meier survival analysis to assess prognosis.
- Conducted Gene Ontology (GO) and KEGG pathway enrichment analyses.
- Examined the relationship between CTDNEP1 expression and the tumor immune microenvironment.
Main Results:
- CTDNEP1 expression is significantly lower in PDAC tissues, particularly in early stages, and associated with key driver gene mutations (KRAS, CDKN2A, TP53, SMAD4).
- Low CTDNEP1 expression correlates with poorer patient prognosis, especially in stage II PDAC.
- Functional enrichment links low CTDNEP1 to autophagy and inflammation, while high expression is associated with mitochondrial function; CTDNEP1 positively correlates with immune cell infiltration.
Conclusions:
- CTDNEP1 acts as a tumor suppressor in PDAC, impacting tumor progression, immune response, and patient survival.
- CTDNEP1 warrants further investigation for its regulatory mechanisms and potential as a therapeutic target or biomarker in PDAC.
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