ArticleFrontiers in cell and developmental biology2025
Integrative pan-cancer analysis of UCP family and experimental validation identifies UCP2 as a potential therapeutic target for glioma.
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- UCP2 Identifies Immunosuppressive Tumor-Associated Macrophages and Is Associated with Predicted Immunotherapy Resistance in Glioma.Oncology research · 2026Article
- Context-dependent roles of UCP2 in cancer: functional heterogeneity, molecular mechanisms and translational perspectives.Frontiers in oncology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To evaluate the prognosis and therapeutic potential of the UCP family, particularly uncoupling protein 2 (UCP2), in 32 types of cancer through integrated analysis of TCGA and CGGA databases. Methods: Multi-omics data from TCGA, CGGA, GTEx, cBioPortal, and ROC Plotter were analyzed to assess UCP family expression patterns, prognostic significance, biological functions, immune cell infiltration, and genetic alterations across various cancers. Results: UCP2 demonstrated significant overexpression in most malignancies, whereas other UCP family members showed reduced expression. High UCP2 expression is a prognostic risk factor for KIRP, LGG, and UVM, while it has protective effects in CESC, OV, SARC, and SKCM. Additional UCP members are associated with enhanced survival in certain cancers, such as BLCA and PAAD. Genetic analysis revealed negative regulation of UCP2 by DNA methylation. Functional enrichment linked the UCP family to epithelial-mesenchymal transition (EMT), G2M checkpoint, UV response, and mitotic processes across cancers. However, in more types of cancer, UCP2 is associated with immune-related pathways. Immune infiltration analysis revealed positive correlations between UCP family expression and stromal/immune scores but negative associations with immunosuppressive cells infiltration. Experimental validation in glioblastoma models confirmed that UCP2 knockdown attenuated EMT, impaired invasion, and improved radiosensitivity. Conclusion: This study establishes UCP2 as a prognostic indicator and potential therapeutic target for glioma.
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