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pmid:40338488

Prostate cancer and metabolic syndrome: exploring shared signature genes through integrative analysis of bioinformatics and clinical data.

Maomao Guo · Sudong Liang · Zhenghui Guan · Jingcheng Mao · Zhibin Xu · Wenchao Zhao · Hao Bian · Jianfeng Zhu · Jiangping Wang · Xin Jin · Yuan Xia

Discover oncology · 2025 doi:10.1007/s12672-025-02561-9

Paper

complete

Experiment

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Data

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Analysis

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absent

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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pmid:40338488
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science-record
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2026-11-01T20:30:30Z
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title
Prostate cancer and metabolic syndrome: exploring shared signature genes through integrative analysis of bioinformatics and clinical data.
doi
10.1007/s12672-025-02561-9
pmid
40338488
authors array · 11 items
[0]
Maomao Guo
[1]
Sudong Liang
[2]
Zhenghui Guan
[3]
Jingcheng Mao
[4]
Zhibin Xu
[5]
Wenchao Zhao
[6]
Hao Bian
[7]
Jianfeng Zhu
[8]
Jiangping Wang
[9]
Xin Jin
[10]
Yuan Xia
journal
Discover oncology
year
2025
abstract
The incidence of both prostate cancer (PCa) and metabolic syndrome (MS) has been steadily increasing due to changes in population structure and lifestyle. These two conditions frequently co-occur, yet their shared pathogenic mechanisms remain unclear. In this study, we utilized bioinformatics and machine learning techniques to analyze public datasets and validated our findings using clinical specimens from our center to identify common signature genes between PCa and MS. We began by screening differentially expressed genes (DEGs) and module genes through Linear models for microarray analysis (Limma) and Weighted Gene Co-expression Network Analysis (WGCNA) of four microarray datasets from the GEO database (PCa: GSE8511, GSE32571, and GSE104749; MS: GSE98895). Comprehensively bioinformatics analyses, including functional enrichment, LASSO, and random forest algorithms, coupled with receiver operating characteristic (ROC) and precision recall curve (PRC) analyses were conducted. We identified 423 DEGs in the PCa dataset and 2481 differentially modular genes in the MS dataset. Among these, 52 intersection genes enriched in immunomodulatory pathways were found. Three common signature genes, namely GPD1L, ACY1, and C12orf75, were identified through LASSO and random forest analyses. Subsequent validation using clinical specimens confirmed differential expression of these genes in PCa, with survival analysis indicating that elevated expression of ACY1 is associated with adverse prognosis in PCa patients. Additionally, immunoinfiltration analysis revealed higher levels of macrophage M0 and activated dendritic cells in PCa tissues. In summary, our study identifies three shared signature genes between PCa and MS, with ACY1 demonstrating adverse prognostic significance in PCa. Our findings provide a foundation for elucidating the pathogenic mechanisms and interplay between PCa and MS, offering novel insights for identifying potential therapeutic targets in PCa.
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We began by screening differentially expressed genes (DEGs) and module genes through Linear models for microarray analysis (Limma) and Weighted Gene Co-expression Network Analysis (WGCNA) of four microarray datasets from the GEO database (PCa: GSE8511, GSE32571, and GSE104749; MS: GSE98895).
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We began by screening differentially expressed genes (DEGs) and module genes through Linear models for microarray analysis (Limma) and Weighted Gene Co-expression Network Analysis (WGCNA) of four microarray datasets from the GEO database (PCa: GSE8511, GSE32571, and GSE104749; MS: GSE98895).
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Publicly available datasets were analyzed in this study. These data can be found at https://www.ncbi.nlm.nih.gov/ geo/(GSE8511, GSE32571, GSE104749 and GSE98895) and https://portal.gdc.cancer.gov/ (TCGA). The code used for analysis and generating the figures in the study can be obtained by contacting the corresponding author.
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Publicly available datasets were analyzed in this study. These data can be found at https://www.ncbi.nlm.nih.gov/ geo/(GSE8511, GSE32571, GSE104749 and GSE98895) and https://portal.gdc.cancer.gov/ (TCGA). The code used for analysis and generating the figures in the study can be obtained by contacting the corresponding author.
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Three common signature genes, namely GPD1L, ACY1, and C12orf75, were identified through LASSO and random forest analyses.
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Three common signature genes, namely GPD1L, ACY1, and C12orf75, were identified through LASSO and random forest analyses.
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Three common signature genes, namely GPD1L, ACY1, and C12orf75, were identified through LASSO and random forest analyses.
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Gene signatures in prostate cancer linked to the Gleason score
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We began by screening differentially expressed genes (DEGs) and module genes through Linear models for microarray analysis (Limma) and Weighted Gene Co-expression Network Analysis (WGCNA) of four microarray datasets from the GEO database (PCa: GSE8511, GSE32571, and GSE104749; MS: GSE98895).
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) and module genes through Linear models for microarray analysis (Limma) and Weighted Gene Co-expres
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-expression Network Analysis (WGCNA) of four microarray datasets from the GEO database (PCa: GSE8511
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w data acquisition and data processing Three microarray datasets (GSE8511, GSE32571, and GSE104749)
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511, GSE32571, and GSE104749) of PCa and one microarray dataset (GSE98895) of MS, including expressi
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signature genes. H Representation images of immunohistochemistry staining for the three signature genes. I Pr
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three signature genes Subsequently, through IHC staining, we observed differential expressio
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We began by screening differentially expressed genes (DEGs) and module genes through Linear models for microarray analysis (Limma) and Weighted Gene Co-expression Network Analysis (WGCNA) of four microarray datasets from the GEO database (PCa: GSE8511, GSE32571, and GSE104749; MS: GSE98895).
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Complete file
{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:40338488", "kind": "science-record", "revision": 4, "content_hash": "sha256:09ad92cd89f2eb605de672dd6d9ffab01c0d5b0ecb1d5294ce3ce308a0974916", "created_at": "2026-11-01T20:30:30Z", "updated_at": "2026-11-01T22:56:30Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Prostate cancer and metabolic syndrome: exploring shared signature genes through integrative analysis of bioinformatics and clinical data.", "doi": "10.1007/s12672-025-02561-9", "pmid": "40338488", "authors": ["Maomao Guo", "Sudong Liang", "Zhenghui Guan", "Jingcheng Mao", "Zhibin Xu", "Wenchao Zhao", "Hao Bian", "Jianfeng Zhu", "Jiangping Wang", "Xin Jin", "Yuan Xia"], "journal": "Discover oncology", "year": 2025, "abstract": "The incidence of both prostate cancer (PCa) and metabolic syndrome (MS) has been steadily increasing due to changes in population structure and lifestyle. These two conditions frequently co-occur, yet their shared pathogenic mechanisms remain unclear. In this study, we utilized bioinformatics and machine learning techniques to analyze public datasets and validated our findings using clinical specimens from our center to identify common signature genes between PCa and MS. We began by screening differentially expressed genes (DEGs) and module genes through Linear models for microarray analysis (Limma) and Weighted Gene Co-expression Network Analysis (WGCNA) of four microarray datasets from the GEO database (PCa: GSE8511, GSE32571, and GSE104749; MS: GSE98895). Comprehensively bioinformatics analyses, including functional enrichment, LASSO, and random forest algorithms, coupled with receiver operating characteristic (ROC) and precision recall curve (PRC) analyses were conducted. We identified 423 DEGs in the PCa dataset and 2481 differentially modular genes in the MS dataset. Among these, 52 intersection genes enriched in immunomodulatory pathways were found. Three common signature genes, namely GPD1L, ACY1, and C12orf75, were identified through LASSO and random forest analyses. Subsequent validation using clinical specimens confirmed differential expression of these genes in PCa, with survival analysis indicating that elevated expression of ACY1 is associated with adverse prognosis in PCa patients. Additionally, immunoinfiltration analysis revealed higher levels of macrophage M0 and activated dendritic cells in PCa tissues. In summary, our study identifies three shared signature genes between PCa and MS, with ACY1 demonstrating adverse prognostic significance in PCa. 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