Research ArticleClinical Studies
Open Access

Low CTDNEP1 Expression Predicts Poor Prognosis and Is Associated With Immune Modulation in Pancreatic Cancer

MAYUKA NII and TADAYOSHI HAYATA
Cancer Genomics & Proteomics January 2026, 23 (1) 144-154; DOI: https://doi.org/10.21873/cgp.20567

Abstract

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.

Keywords:

Introduction

Pancreatic cancer, especially pancreatic ductal adenocarcinoma (PDAC), is a devastating malignancy characterized by aggressive local invasion and early metastasis (1, 2). It is among the deadliest cancers, with incidence and mortality rates steadily rising. A significant clinical challenge lies in the late-stage diagnosis of most patients, often due to the absence of early symptoms and the lack of reliable biomarkers. Therefore, identifying novel genes implicated in PDAC progression is a critical unmet need.

CTD nuclear membrane phosphatase 1 (CTDNEP1) is a gene encoding a phosphatase (3). Studies in mice have demonstrated that Ctdnep1 deficiency leads to enhanced BMP and TGF-β signaling, resulting in renal failure (4), ovarian hemorrhage (5), and delayed bone formation (6). Furthermore, emerging evidence suggests a link between CTDNEP1 deficiency and the development of medulloblastoma, a pediatric brain tumor, hinting at a potential tumor suppressor role (7-9). However, the role of CTDNEP1 in other malignant tumors, including PDAC, remains largely unknown. This study aimed to investigate the expression and clinical significance of CTDNEP1 in PDAC using multi-omics data from the TCGA Pan-Cancer Atlas. We further analyzed the molecular pathways and interaction networks associated with CTDNEP1 to elucidate the potential mechanisms underlying its role in pancreatic tumor progression.

Materials and Methods

Analysis of the pancreatic ductal adenocarcinoma [The Cancer Genome Atlas (TCGA), Pan-Cancer Atlas)] dataset. The TCGA and Pan-Cancer Atlas datasets (n=184) (10, 11) were downloaded from cBioPortal (https://www.cbioportal.org/) (12, 13) on March 8, 2025. Expression data for CTDNEP1 in normal tissue and primary tumors not derived from the same patient were downloaded from TIMER2.0 (https://compbio.cn/timer2/) (14), and UALCAN (https://ualcan.path.uab.edu/index.html) (15, 16).

Statistical analysis. Statistical analysis was performed using R software (version 4.4.0, R Foundation, Vienna, Austria). The TCGA and Pan-Cancer Atlas datasets included gene mutation data, mRNA expression levels in primary pancreatic cancer samples (n=177), overall survival (OS) (n=177), disease-specific survival (DSS) (n=171), disease-free survival (DFI) (n=69), progression-free survival (PFI) (n=177), gene mutations (n=177), and copy number mutations (n=176). Optimal cutoff values for classifying patients into high-expression and low-expression groups were determined using R (OS: 2025.215, DSS: 2025.215, DFI: 2082.165, PFI: 2083.630). Survival curves for OS, DSS, DFI, and PFI were generated using the Kaplan-Meier method and compared using the log-rank test. A two-sided p<0.05 was considered statistically significant.

Immune infiltration analysis. Using the TIMER2.0 database (https://compbio.cn/timer2/), we evaluated the correlation between CTDNEP1 expression and the infiltration of immune cells (dendritic cells, neutrophils, macrophages, CD4+ T cells, CD8+ T cells, and B cells) in pancreatic cancer.

Differential gene expression analysis and functional enrichment analysis. To elucidate the biological functions associated with CTDNEP1 expression, samples were classified into high-expression and low-expression groups based on median CTDNEP1 expression. GO enrichment and KEGG pathway analysis were performed using R. Enriched terms with an adjusted p-value <0.05 were considered statistically significant.

Results

Low CTDNEP1 expression is associated with poor prognosis in PDAC. Previous studies have reported that low CTDNEP1 expression is associated with poor prognosis in medulloblastoma, a malignant brain tumor in children (7-9). To explore the potential of CTDNEP1 as a prognostic marker in other cancers, we investigated its expression across various tumor types. The study design is outlined in Figure 1A. To evaluate CTDNEP1 expression across human cancers, we used the TIMER2.0 database to confirm the difference in CTDNEP1 expression between adjacent normal tissue and tumors in all TCGA tumors. As shown in Figure 1B, CTDNEP1 expression was significantly lower in tumors compared to normal tissue in multiple cancers, including pancreatic cancer. We, therefore, focused our study on CTDNEP1 expression in PDAC. We next examined CTDNEP1 expression by tumor stage. The results showed that CTDNEP1 expression was already significantly reduced in stage I compared to normal tissue (Figure 1C).

Figure 1.
Figure 1.
Figure 1.

Differences in CTDNEP1 expression levels between normal and tumor tissues, and during tumor stages. (A) The study’s flow chart. (B) CTDNEP1 expression levels in pan-cancer from the TCGA database using TIMER2.0. (*p<0.05, **p<0.01, ***p<0.001). (C) CTDNEP1 expression levels by tumor stage using UALCAN.

Low CTDNEP1 expression is associated with driver gene mutations in KRAS, CDKN2A, TP53, and SMAD4 in PDAC. The progression of PDAC is known to involve a multistep carcinogenesis process driven by sequential mutations in genes such as KRAS, CDKN2A, TP53, and SMAD4 (17). We, therefore, investigated the relationship between mutations in these key driver genes and CTDNEP1 expression (Figure 2A-D). PDAC tumors harboring KRAS missense mutations, including G12D, G12V, G12R, and G12C, exhibited significantly reduced CTDNEP1 expression compared to KRAS wild-type tumors (Figure 2A). Similarly, TP53 missense and truncation mutations were also associated with reduced CTDNEP1 expression (Figure 2C). Furthermore, PDAC tumors with significant deletions of CDKN2A, TP53, or SMAD4 showed decreased CTDNEP1 expression compared to tumors with two copies of these genes (Figure 2E-H). Given that KRAS missense mutations often occur early in PDAC development, these results suggest that the reduction in CTDNEP1 expression may be an early event in PDAC progression.

Figure 2.
Figure 2.

Association between CTDNEP1 expression and gene mutations or copy number alterations in KRAS, CDKN2A, TP53 and SMAD4. (A-H) Beeswarm plots showing the association between CTDNEP1 expression and driver gene status. (A-E) CTDNEP1 gene expression compared to copy number alterations in (A) KRAS, (B) CDKN2A, (C) TP53 and (D) SMAD4 gene mutations (wild-type, missense, inframe, truncating, splice and multiple). (E-H) CTDNEP1 expression compared with copy number changes of (E) KRAS, (F) CDKN2A, (G) TP53 and (H) SMAD4. KRAS: KRAS proto-oncogene; CDKN2A; cyclin-dependent kinase inhibitor 2A; TP53: tumor protein p53; SMAD4: SMAD family member 4; N.S.: not significant.

Low CTDNEP1 expression is associated with poor prognosis in stage II PDAC. To investigate the association between CTDNEP1 gene expression and prognosis at different tumor stages, we performed Kaplan-Meier analysis using OS, DSS, DFI, and PFI as endpoints. Kaplan-Meier analysis revealed that patients in the CTDNEP1 low-expression group had a poorer prognosis compared to those in the CTDNEP1 high-expression group (OS: p=0.00082, DSS: p=0.0051, DFI: p=0.047, PFI: p=0.053) (Figure 3A-D). These results indicate that low CTDNEP1 expression is associated with poor prognosis and contributes to recurrence and progression of pancreatic cancer. Notably, in the Kaplan-Meier analysis of stage I tumors, no significant differences in survival were observed between the CTDNEP1 high-expression and low-expression group (OS: p=0.57, DSS: p=0.85, DFI: p=0.76, PFI: p=0.32) (Figure 3E-H). However, in stage II tumors, patients with low CTDNEP1 expression had significantly worse overall and disease-specific survival compared to those with high CTDNEP1 expression (OS: p=0.0078, DSS: p=0.026, DFI: p=0.32, PFI: p=0.56) (Figure 3I-L). No significant differences were observed for DFI and PFI in stage II (Figure 3K-L). Due to insufficient case numbers, survival analysis could not be performed for stages III and IV. These results suggest that CTDNEP1 plays a role in cancer progression specifically in stage II PDAC, with low CTDNEP1 expression associated with worse outcomes.

Figure 3.
Figure 3.

Kaplan-Meier analyses of differences in OS, DSS, DFI and PFI between CTDNEP1 high and CTDNEP1 low groups of patients in pancreatic cancer. The Cancer Genome Atlas Pan-Cancer data was downloaded from cBioPortal. (A-D) All patients with pancreatic cancer: (A) OS, (B) DSS, (C) DFI and (D) PFI. (E-H) Patients at stage I: (E) OS, (F) DSS, (G) DFI and (H) PFI. (I-L) Patients at stage II: (I) OS, (J) DSS, (K) DFI and (L) PFI. OS: Overall survival; DSS: disease-specific survival; DFI: disease-free interval; PFI: progression-free interval; CTDNEP1 high: patients with high expression of CTDNEP1; CTDNEP1 low: patients with low expression of CTDNEP1.

GO and KEGG pathway enrichment analysis. To gain insights into the biological processes and signaling pathways associated with CTDNEP1 expression in pancreatic cancer, we performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses using transcriptome data from the TCGA-PAAD dataset. Patients were classified into high-expression and low-expression groups based on CTDNEP1 expression. Differential expression analysis identified genes differentially expressed between the two groups, and functional enrichment analysis was performed on these genes. In the CTDNEP1 low-expression group (Figure 4A-B), GO enrichment analysis revealed that the differentially expressed genes were mainly enriched in biological processes such as macroautophagy, endosome transport, proteasome-mediated ubiquitin-dependent protein process, protein polyubiquitination, and viral process (Figure 4A). KEGG pathway analysis in this group showed enrichment of infection- and immune-related pathways, including Hepatitis C, endocytosis, ubiquitin-mediated proteolysis, NOD-like receptor signaling pathways, and PD-L1 expression and PD-1 checkpoint pathways in cancer (Figure 4B). This suggests that activation of immune and inflammatory responses may occur in tumors with low CTDNEP1 expression. In contrast, in the CTDNEP1 high-expression group (Figure 4C-D), GO enrichment analysis showed ribosome biogenesis, mitochondrial translation, oxidative phosphorylation, and electron transport chain (Figure 4C), suggesting enhanced mitochondrial and biosynthetic activity. KEGG pathway analysis in the high-expression group was mainly enriched in neurodegenerative disease pathways such as Parkinson disease, Huntington disease, and Alzheimer disease, oxidative phosphorylation, Coronavirus disease-COVID-19, and non-alcoholic fatty liver disease (Figure 4D). These pathways are closely related to mitochondrial metabolism, oxidative stress response, and energy production. These results suggest that low expression of CTDNEP1 in pancreatic cancer promotes protein degradation and immune/inflammatory pathways, while high expression is associated with improved mitochondrial function, ribosomal biosynthesis, and metabolic activity.

Figure 4.
Figure 4.

GO and KEGG pathway enrichment analyses based on CTDNEP1 expression in pancreatic cancer. (A) GO enrichment analysis in the CTDNEP1 low expression group. (B) KEGG pathway analysis in the CTDNEP1 low expression group. (C) GO enrichment analysis in the CTDNEP1 high expression group. (D) KEGG pathway analysis in the CTDNEP1 high expression group. The color scale represents statistical significance (log10 of adjusted p-value), and the length of the bars indicates the number of genes enriched in each term or pathway. The color scale represents the statistical significance (−log10 adjusted p-value), and the length of the bars indicates the number of genes enriched in each term or pathway. GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes.

CTDNEP1 expression correlates with immune cell infiltration in PDAC. We used TIMER2.0 to investigate the potential role of CTDNEP1 in immune cell infiltration (B cells, CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells) (Figure 5). The results showed that CTDNEP1 expression was positively correlated with CD4+ T cells (partial correlation coefficient=0.366, p=1.02×10−6), macrophages (partial correlation coefficient=0.51, p=1.09×10−12), neutrophils (partial correlation coefficient=0.316, p=2.52×10−5), and dendritic cells (partial correlation coefficient=0.306, p=4.77×10−5). These findings suggest that CTDNEP1 may be associated with the infiltration of immune cells in pancreatic cancer and that CTDNEP1 expression can influence the composition of the tumor’s immune microenvironment. Therefore, low CTDNEP1 expression may contribute to tumor malignancy through immune evasion mechanisms or chronic inflammation, while high CTDNEP1 expression may be associated with a metabolically active tumor environment with lower immune suppression.

Figure 5.
Figure 5.

The association between CTDNEP1 expression and immune cell infiltration (B cells, CD8+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells).

Discussion

This study demonstrated that CTDNEP1 expression is significantly reduced in PDAC and is associated with the mutation status of major driver genes such as KRAS, CDKN2A, TP53, and SMAD4. These results suggest that CTDNEP1 low expression occurs early in pancreatic cancer and may play a role in disease progression and malignancy. Previous reports have shown that CTDNEP1 expression is reduced in medulloblastoma, suggesting its potential role as a tumor suppressor gene (7-9). Consistent with these findings, our analysis using TCGA and publicly available datasets confirmed that CTDNEP1 expression is significantly reduced in PDAC tissues compared to adjacent normal tissues, and this reduction was clearly observed even in tumors at the early stage of stage I. Furthermore, the reduction in CTDNEP1 expression was significantly associated with major driver mutations in KRAS and TP53, as well as deletions in CDKN2A and SMAD4. The prognostic relevance of CTDNEP1 expression was demonstrated by Kaplan-Meier survival analysis. This analysis showed that patients with CTDNEP1 low expression had significantly poorer OS, DSS, DFI, and PFI compared to patients with high expression. The poor prognosis in the CTDNEP1 low expression group, particularly in stage II, suggests that this gene may function as a prognostic biomarker in PDAC. Functional enrichment analysis provided further insights into the molecular mechanisms associated with CTDNEP1 expression. CTDNEP1 low expression was suggested to be associated with the upregulation of processes related to macroautophagy, the ubiquitin-dependent protein process, and immune response. In contrast, in the high-expression group, processes related to ribosome biogenesis, mitochondrial translation, and oxidative phosphorylation were enriched.

The tumor microenvironment (TME) plays an important role in cancer recurrence and drug resistance (18). Immune cells within the TME, such as CD4+ T cells and CD8+ T cells, are associated with the efficacy of immunotherapy (19). Our immune infiltration analysis revealed a positive correlation between CTDNEP1 expression and the infiltration of multiple immune cells, including CD4+ T cell, macrophages, neutrophils, and dendritic cells. These results suggest that CTDNEP1 may play a role in regulating the tumor immune microenvironment.

Several other genes and pathways have been implicated in PDAC progression and immune evasion, demonstrating the complex interplay of factors influencing this disease. For example, dysregulation of the transforming growth factor-beta (TGF-β) signaling pathway, known to be influenced by CTDNEP1 in other contexts (4-6), has also been shown to promote PDAC progression and suppress anti-tumor immunity. Similarly, alterations in autophagy, another process linked to CTDNEP1 in our study, have been demonstrated to contribute to both tumor cell survival and immune modulation in PDAC (20, 21). Therefore, our findings suggest that CTDNEP1 may represent a novel node in the complex network of pathways that govern PDAC pathogenesis and the tumor-immune interaction.

While this study provides compelling evidence for the role of CTDNEP1 in PDAC, there are certain limitations that warrant consideration. Firstly, our analysis relies on retrospective data from the TCGA database. Although the TCGA dataset is a valuable resource, it is subject to inherent biases and limitations in data collection and patient follow-up. Secondly, our sample size for survival analysis in stages III and IV PDAC was insufficient to draw definitive conclusions. Thirdly, while we demonstrate a correlation between CTDNEP1 expression and immune cell infiltration, further functional studies are needed to elucidate the precise mechanisms by which CTDNEP1 influences the tumor immune microenvironment. Future studies should also focus on validating these findings in independent PDAC cohorts and exploring the therapeutic potential of targeting CTDNEP1 in this aggressive malignancy.

In conclusion, the results of this study suggest that CTDNEP1 may function as a tumor suppressor in PDAC. Future studies should elucidate the detailed regulatory mechanisms of CTDNEP1 and evaluate its potential as a therapeutic target or biomarker in PDAC and other cancers.

Conclusion

This study identifies CTDNEP1 as a potential tumor suppressor in pancreatic cancer, with its low expression linked to poor survival outcomes and modulation of the tumor immune microenvironment.

Footnotes

  • Conflicts of Interest

    The Authors declare no potential conflicts of interest.

  • Authors’ Contributions

    All Authors contributed to the conception and design of the study. MN performed data collection and analysis. MN prepared the draft, which was revised by TH. All Authors read and approved the final manuscript.

  • Artificial Intelligence (AI) Disclosure

    During the preparation of this manuscript, a large language model (Google Gemini) was used solely for language editing and stylistic improvements in select paragraphs. No sections involving the generation, analysis, or interpretation of research data were produced by generative AI. All scientific content was created and verified by the authors. Furthermore, no figures or visual data were generated or modified using generative AI or machine learning–based image enhancement tools.

  • Received September 16, 2025.
  • Revision received October 21, 2025.
  • Accepted November 3, 2025.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY-NC-ND) 4.0 international license (https://creativecommons.org/licenses/by-nc-nd/4.0).

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Low CTDNEP1 Expression Predicts Poor Prognosis and Is Associated With Immune Modulation in Pancreatic Cancer
MAYUKA NII, TADAYOSHI HAYATA
Cancer Genomics & Proteomics Jan 2026, 23 (1) 144-154; DOI: 10.21873/cgp.20567
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