ArticleInternational journal of molecular sciences2025
BST2 and DIRAS3 Drive Immune Evasion and Tumor Progression in High-Grade Glioma.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- A structural bioinformatics framework for prioritizing pH-sensitive proteins from 3D structural features.BMC bioinformatics · 2026Article
- Emerging Oncogenic and Immunoregulatory Roles of BST2 in Human Cancers.Biomedicines · 2026Review
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Authors and funding
6 authors.
Funding
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Abstract
High-grade gliomas (HGGs, WHO grades 3-4) are highly aggressive, with a poor prognosis and treatment resistance. Immune evasion may contribute to their progression, but the role of cytotoxic T-lymphocyte immune evasion (CTLE) is not well-validated. This study analyzed the transcriptomic data of 525 patients from TCGA-GBM-HG_U133A. Two molecular subtypes were identified based on 182 CTLE-associated genes, with 238 differentially expressed genes between them. A prognostic model was developed, identifying BST2 and DIRAS3 as key risk factors, and validated in multiple cohorts. The subtypes had distinct immune profiles, with Cluster 2 showing higher immune infiltration but a poorer prognosis. The model had a good predictive performance. High-risk patients had upregulated BST2 and DIRAS3, linked to immunosuppression and shorter survival. Knockdown experiments confirmed their roles in GBM cell migration and invasion. Mechanistically, they promote immune evasion. BST2 and DIRAS3 could be therapeutic targets for HGG immunotherapy.
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