ArticleMedical oncology (Northwood, London, England)2026
Identification of a lncRNA prognostic signature reveals that SNAI3-AS1 cooperates with erastin to reshape macrophage polarization in glioma.
Article in Medical oncology (Northwood, London, England), 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
Glioma progression is heavily driven by heterogeneity and a highly immunosuppressive tumor microenvironment (TME). This study aimed to identify a robust long non-coding RNA (lncRNA) prognostic signature and elucidate its role in TME remodeling. An unbiased transcriptome-wide screening of the TCGA and CGGA databases was performed. A prognostic risk signature was constructed using univariate and multivariate Cox regression. Based on multivariate coefficients, the core protective gene SNAI3-AS1 was selected for in vitro validation in U87 and U251 cells. Additionally, a U87-derived conditioned medium (CM) co-culture system was established to investigate the cooperative reinforcement of SNAI3-AS1 overexpression and the ferroptosis inducer erastin on macrophage polarization (THP-1 cell line), assessed via RT-qPCR and ELISA. A 23-lncRNA prognostic signature was established, demonstrating high accuracy in predicting overall survival and correlating positively with immunosuppressive M2 macrophage infiltration. RT-qPCR results revealed that SNAI3-AS1 was significantly downregulated in glioma tissues. While SNAI3-AS1 overexpression did not alter cell proliferation, it profoundly suppressed three-dimensional matrix migration and invasion. Moreover, SNAI3-AS1 overexpression cooperates with erastin to elevate cellular levels of malondialdehyde and Fe
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