ArticleAnnals of medicine2025
Unveiling the prognostic and immunological role of IFI44 in glioma.
Article in Annals of medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- IFI44 Orchestrates an IL-10-Driven M2 Macrophage Program in Breast Cancer: An Immune Prognostic Signature.Breast cancer (Dove Medical Press) · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGliomas are aggressive central nervous system tumors with limited understanding of their molecular drivers. Identifying novel prognostic and therapeutic biomarkers remains crucial.
methodsUsing TCGA, GTEx, GEO, and CGGA datasets, we performed differential expression, Cox regression, and LASSO analyses to identify prognostic genes. IFI44, one of eight significant candidates, was analyzed for its association with survival, clinical features (IDH mutation, 1p/19q codeletion) and tumor immune microenvironment. Functional assays were conducted to evaluate its effects on glioma cell proliferation, migration, and invasion.
resultsTranscriptomic analysis of 1,142 normal and 398 glioma samples identified 61 consistently dysregulated genes, predominantly enriched in immune-related rather than classical oncogenic pathways. In CGGA cohorts, eight progression-associated genes were identified, six associated with poor prognosis. IFI44 expression correlated with higher grade, older age, IDH wild type, and 1p/19q non-codeletion. High IFI44 tumors were enriched for NF1 mutations, while low IFI44 tumors carried IDH1, NOTCH1, and CIC mutations. Mechanistically, IFI44-high gliomas exhibited immune-suppressive pathway enrichment, increased checkpoint expression (PD-1/PD-L1, CTLA4, LAG3), and macrophage infiltration. Protein interaction analysis linked IFI44 to cytokine signaling and T-cell regulation. In U87 and U251 cells, IFI44 overexpression promoted proliferation, migration, and invasion, whereas knockdown suppressed these phenotypes.
conclusionsIFI44 may drive glioma progression through dual mechanisms of immune microenvironment remodeling and promotion of tumor cell aggressiveness, supporting its potential as a prognostic biomarker and therapeutic target. Although preliminary knockdown and overexpression assays were performed, the underlying mechanisms of IFI44-mediated immune regulation and tumor progression require further investigation.
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