ArticleBMC cancer2025
Systematic analysis identifies TRIM22 as an oncogenic and immunological biomarker in glioma.
Article in BMC cancer, 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.
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
1 citing paper in PubMed.
- TRIM22 in cancer: a context-dependent E3 ligase at the interface of interferon, p53, and tumor plasticity.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
The regulatory role of tripartite motif-containing 22 (TRIM22) has been reported in multiple types of cancers and disease, however, its potential role in gliomas remains poorly understood. In this study, we aimed to elucidate the biological role of TRIM22 in gliomas. The expression levels of TRIM22 in tumors were analyzed in datasets of The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx). The clinical prognosis of TRIM22 was evaluated by clinical survival data of TCGA cohort and validated by Chinese Glioma Genome Atlas cohort (CGGA). The correlations between TRIM22 expression and immune scores, immune cell infiltration, and immune checkpoint genes were conducted. The genes positively and negatively co-expressed with TRIM22 were identified using TCGA data to explore the functions and pathways affected by TRIM22 in glioma. Cell proliferation assay, migration assay, and apoptosis assay were used to interrogate the function of TRIM22 in glioma. TRIM22 expression was significantly increased in glioma with higher malignancy and predicted poor outcomes. TRIM22 expression was associated with tumor immune microenvironment in glioma. Gene Ontology (GO)/ Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that TRIM22 was involved in the regulation of cell-cell adhesion. Finally, the suppression of TRIM22 resulted in inhibition of proliferation and migration with increased cell apoptosis in T98G and U251 glioma cells. In summary, TRIM22 acts as a potential oncogenic factor and prognostic biomarker in glioma. Although preliminary evidence points to its role in immune regulation, further mechanistic and in vivo validation studies are warranted to clarify its immunomodulatory functions.
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