ArticleCell death & disease2026
Targeting the tumor microenvironment: reprogramming macrophages as a novel therapeutic strategy in FUOM-deficient glioblastoma.
Article in Cell death & disease, 2026. 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.
- Plasma proteomics framework predicts metabolic dysfunction-associated steatotic liver disease up to 16 years before onset.Nature aging · 2026Article
- Glioma-derived extracellular vesicles as drivers of immunotherapeutic resistance: mechanisms of immune reprogramming and metabolic intervention.Frontiers in immunology · 2026Review
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Authors and funding
8 authors.
Funding
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Abstract
Glioma, the most prevalent CNS malignancy and generally poor prognosis, is characterized by a highly immunosuppressive tumor microenvironment. Fucose mutarotase (FUOM) is a known rockulose mutase secretion protein involved in pathological immune remodeling. However, the precise role of FUOM involvement in glioma has yet to be elucidated. Herein, we delineated FUOM expression using multiplex-immunohistochemistry on tissue microarrays, and its prognostic predictive value was assessed using the Cox regression method. Then we investigated the altered proliferation, migration, and invasion capabilities of glioma cells upon regulated FUOM expression in vitro. Chemokine antibody microarray, immunoassay, and Co-IP were employed to detect interactions between macrophages and glioma cells. In addition, the in vivo therapeutic effects of FUOM were confirmed using animal subcutaneous glioma models. FUOM was highly expressed in glioma tissues and correlated with aggressive glioma progression and unfavorable patient prognosis. Macrophage infiltration into the glioma TME was observed upon FUOM downregulation, with induced CXC motif chemokine ligand-13 (CXCL13) release in maintaining M2-like phenotype. In addition, conditioned media from FUOM knockdown glioma cell lines induced M2-like macrophage chemotaxis migration. Finally, blocking FUOM expression on glioma models enhanced M2-like macrophage phenotype and increased chemotactic migration both in vivo and in vitro. Collectively, our work reveals that FUOM induces M2-like macrophage polarization and promotes glioma progression by mediating CXCL13 secretion.
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