ArticleDiscover oncology2025
Comprehensive pan-cancer analysis of ENOPH1 in human tumors.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Comprehensive pan-cancer analysis of MEX3A in human tumors.Discover oncology · 2026Article
- A pan-cancer analysis of MEX3D in human tumors.Discover oncology · 2026Article
- Comprehensive pan-cancer analysis of MEX3C in human tumors.Discover oncology · 2026Article
- Comprehensive bioinformatics analysis of EXOSC family genes in lung adenocarcinoma.Discover oncology · 2026Article
- A pan-cancer analysis of TMEM132A in human tumors.Discover oncology · 2026Article
- Comprehensive bioinformatics analysis of MEX3 family genes in hepatocellular carcinoma.Scientific reports · 2025Article
- Expression patterns, prognostic significance, and immune correlations of the TNFAIP8 family in acute myeloid leukemia: a comprehensive bioinformatics analysis.Discover oncology · 2025Article
- Integrative bioinformatic and experimental analysis reveals prognostic and immunological roles of MEX3 family genes in glioma.Frontiers in immunology · 2025Article
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5 authors.
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Abstract
backgroundENOPH1 (Enolase-phosphatase 1), a member of the HAD-like hydrolase superfamily, has been linked to a range of physiological conditions, including neurological disorders. However, its involvement in tumorigenesis remains underexplored. This study is the first to conduct a pan-cancer analysis of ENOPH1, aiming to elucidate its role in multiple cancers through various bioinformatics platforms.
methodsWe conducted a thorough analysis using data from UCSC databases. ENOPH1 expression in tumor and normal tissues was evaluated using R language software. Survival analyses, genetic alterations, and RNA modifications were assessed through the GEPIA2 and cBioPortal platforms. The relationships between ENOPH1 and immune infiltration, tumor mutational burden (TMB), microsatellite instability (MSI), and homologous recombination deficiency (HRD) were examined using TIMER2 and R software. ENOPH1-related gene enrichment analysis was performed using the STRING and GEPIA2 databases, followed by Gene Ontology (GO) and KEGG pathway enrichment analyses.
resultsENOPH1 expression was significantly upregulated in various cancers, including ACC, BLCA, BRCA, and COAD. High ENOPH1 expression was associated with poor overall survival (OS) in cancers such as KICH, LIHC, BRCA and LUAD. High ENOPH1 expression was associated with poor disease specific survival (DSS) in cancers such as KICH, LIHC, BRCA and MESO. Genetic alterations of ENOPH1, primarily mutations and deep deletions, were identified in UCEC, BLCA, and OV. ENOPH1 showed significant correlations with RNA modifications (m1A, m5C, m6A), immune checkpoints, and immune modulators across multiple cancer types. ENOPH1 was positively correlated with TMB, MSI, and HRD in cancers like BLCA, BRCA, and STAD. Furthermore, enrichment analysis revealed that ENOPH1 interacts with proteins involved in critical pathways such as AMPK, Hippo, and PI3K-AKT, suggesting its role in cancer progression.
conclusionThis pan-cancer analysis reveals ENOPH1's potential as a prognostic biomarker and its involvement in key signaling pathways across multiple cancers. Our findings provide new insights into the role of ENOPH1 in tumorigenesis and highlight its potential as a therapeutic target in cancer treatment.
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