ArticleApplied biochemistry and biotechnology2026
CXCL8 Enhances Malignancy of GBM via TNFα-NFκB Mediated Suppression of Ferroptosis.
Article in Applied biochemistry and biotechnology, 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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Abstract
Glioblastoma (GBM) is a lethal type of brain tumor characterized by heterogeneity in the tumor microenvironment (TME); however, despite the implementation of comprehensive standard therapy, the prognosis of GBM patients remains dismal. Recent studies have shown that targeting ferroptosis and chemokines could provide potential insights for treating tumors, but relevant studies on GBM are lacking. Ferroptosis-related genes associated with GBM were downloaded from FerrDb V2, and the status of ferroptosis was clarified. Differentially expressed genes (DEGs) were analyzed, and CXCL8 was selected for subsequent validation. The transcriptomic profiles of GBM were downloaded from the Gene Expression Omnibus (GEO), and single-cell analysis and spatial transcriptomics were performed to determine the biological functions of the sub-cell types. The mediated pathway was subjected to gene set enrichment analysis (GSEA) and validated through staining and transmission electron microscopy (TEM). In this study, we demonstrated the heterogeneity of ferroptosis in GBM and constructed an optimal nomogram. CXCL8 was proven to be significantly correlated with the degree of ferroptosis. With respect to the TME of GBM, spatial transcriptomics revealed that MES-like cells and CXCL8 + tumor-associated macrophages (TAMs) share the same location of ferroptosis. We further found that TNFα-NFκB mediated the activity of CXCL8 and suppressed ferroptosis, leading to the malignant biological behavior of GBM cells. The CXCL8-TNFα-NFκB axis restrains the TME of ferroptosis and leads to poor prognosis in GBM patients, indicating that it is a potential biological mechanism for GBM.
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