ArticleFrontiers in immunology2026
Cross-scale modeling reveals a TFRC-driven immunosuppressive macrophage niche in cervical cancer.
Article in Frontiers in immunology, 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
Background: The functional plasticity of tumor-associated macrophages (TAMs) is a critical determinant of the immunosuppressive microenvironment in cervical cancer, yet its integration into actionable prognostic frameworks remains limited. This study aimed to establish a TAM polarization-centered model and elucidate the mechanisms of underlying tumor-immune crosstalk. Methods: Bulk transcriptomics from The Cancer Genome Atlas (TCGA) were integrated with single-cell RNA sequencing (scRNA-seq) data (GSE208653). By combining weighted gene co-expression network analysis (WGCNA) with a multi-algorithm machine learning framework, a prognostic signature was constructed and independently validated in the Gene Expression Omnibus (GEO) GSE52903 cohort. Single-cell analysis resolved the cellular origins of signature genes, prioritizing tumor-enriched genes for validation. Protein-level expression was verified via immunohistochemistry (IHC) in a paired clinical cohort (n=39). Functional validation of the core gene was performed Results: A robust five-gene prognostic signature (TP73, TFRC, SHC1, SCD, and PFKFB3) was developed, effectively stratifying patient survival. High risk scores correlated with a suppressed antitumor immune landscape and diminished predicted chemosensitivity to agents such as cisplatin. Single-cell analysis and IHC confirmed transferrin receptor (TFRC) as a tumor-intrinsic factor that is progressively upregulated during cervical carcinogenesis and enhances pro-M2 signaling. Conclusions: This study establishes a cross-scale, biologically interpretable prognostic model linking macrophage plasticity to clinical outcomes. We identify TFRC as a pivotal metabolic-immune node through which tumor-intrinsic iron metabolism orchestrates an immunosuppressive niche, providing a foundation for novel therapeutic strategies in cervical cancer.
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