ReviewFrontiers in oncology2026
Metabolic remodeling and immune evasion in glioblastoma: a focus on serine and lipid networks.
Review in Frontiers in oncology, 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
4 authors.
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Abstract
Glioblastoma (GBM) is a highly aggressive brain tumor characterized by metabolic plasticity that fuels growth, therapy resistance, and immune evasion. Among its reprogrammed pathways, serine and lipid metabolism play central roles. The serine synthesis pathway (SSP)-via PHGDH, PSAT1, and SHMT2-supports nucleotide biosynthesis, redox balance, and epigenetic regulation, especially under hypoxic and nutrient-deprived conditions. Meanwhile, fatty acid flux, FABP7-mediated PUFA transport, and cholesterol uptake reshape the tumor microenvironment, sustain glioma stemness, and promote immune suppression. Key lipid enzymes and ferroptosis regulators such as MAGL, ACSL4, and xCT modulate tumor survival and therapy response. GBM cells also exhibit high reliance on exogenous cholesterol, with dysregulation of LXR-SREBP pathways and mevalonate flux contributing to autophagy and proliferation. Therapeutic strategies targeting metabolic vulnerabilities-including SSP blockade, cholesterol homeostasis disruption, and ferroptosis induction-show synergistic effects with conventional agents like temozolomide. This review highlights the intertwined metabolic circuits in GBM and explores their translational potential as targets for precision therapy.
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