ArticleOncogene2026
Enhancing glioma immunotherapy by disrupting RBP-J-mediated NNMT signaling in tumor microenvironment.
Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Authors and funding
7 authors.
Funding
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Abstract
Glioma is a highly aggressive central nervous system malignancy characterized by profound immune evasion, the underlying mechanisms of which remain incompletely defined. This study investigated how the transcription factor RBP-J drives immune suppression through activation of NNMT in cancer-associated fibroblasts (CAFs). By integrating single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST), we identified a CAF-specific NNMT-high subpopulation enriched at the tumor margin and closely associated with M2 macrophages. Bioinformatic analyses using Seurat and Monocle3 delineated a stromal-immune regulatory network and highlighted RBP-J as a potential upstream regulator of NNMT. Mechanistic experiments demonstrated that RBP-J directly binds to the NNMT promoter and activates its transcription, leading to intracellular SAM depletion, reduced H3K27me3 levels, and epigenetic upregulation of SAA3. Elevated SAA3 promoted M2 macrophage recruitment and polarization, resulting in CD8
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Registered trials
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