ArticleDiscover oncology2026
A five-gene TAM and MYCN signature predicts prognosis and identifies MTHFD2 as a therapeutic target in neuroblastoma.
Article in Discover 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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Abstract
backgroundTumor-associated macrophages (TAMs) are key components of the tumor immune-suppressive microenvironment. However, studies focusing on the modulation of TAM-specific gene signatures to improve neuroblastoma (NB) prognosis are limited. MYCN amplification (MNA) is known to influence the immune landscape in neuroblastoma.
methodsSingle-cell sequencing of 19 NB samples and transcriptome data from 498 NB samples were analyzed to identify macrophage-specific genes associated with poor NB prognosis. A risk signature was constructed by integrating differentially expressed genes (DEGs) related to TAMs and MYCN using univariate Cox regression, LASSO regression, and Kaplan-Meier survival analysis. Single-factor and multi-factor Cox regression analyses were conducted to explore the relationship between clinical characteristics and prognosis, and a nomogram was constructed. The impact of downregulating TAM target genes in macrophages was explored using CCK8, EdU incorporation, and Transwell assays.
resultsA signature based on five macrophage-related genes associated with NB prognosis (FCGR3A, ATF5, MTHFD2, HMGA1, and LY6E) was successfully established and validated for its strong prognostic predictive performance (AUC: 0.829). A clinically applicable Nomogram incorporating these genes was also developed. CCK-8 assays revealed a time-dependent inhibitory effect on neuroblastoma cell proliferation upon co-culture with MTHFD2-knockdown macrophages. EdU and Transwell assays showed that downregulation of MTHFD2 in macrophages significantly reduced the invasive and migratory capabilities of NB cells, particularly in MYCN-amplified cells.
conclusionWe developed and validated a five-gene signature based on TAM and MYCN-related genes with strong prognostic performance. Downregulation of MTHFD2 in macrophages reduced neuroblastoma cell proliferation, invasion, and migration, particularly in MYCN-amplified cells, highlighting MTHFD2 as a potential therapeutic target in high-risk patients.
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