ArticleMolecular biology reports2026
Single-cell transcriptomic analysis of macrophage heterogeneity and tumor-associated candidate genes in prostate cancer.
Article in Molecular biology reports, 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
backgroundProstate cancer (PCa) progression is closely linked to tumor-associated macrophage (TAM) heterogeneity, but functional diversity of TAM subsets beyond the classical M1/M2 framework remains insufficiently characterized. METHODS AND
resultsUsing scRNA-seq on tumor (n = 5) and adjacent-normal tissues (n = 3) from six PCa patients, we analyzed macrophage subclusters via pseudotime, hdWGCNA, random forest, and CellChat. We identified a tumor-enriched, late-pseudotime macrophage subset showing active NF-κB signaling, elevated inflammatory cytokines (IL1B, TNF), and intensified CCL3, TNF, and SPP1 intercellular signaling. hdWGCNA revealed a disease-correlated module (r = 0.9, FDR < 0.1), from which three candidate genes (CALU, ARID1B, MARF1) were identified. In a THP-1/PC-3 co-culture model, all three genes were upregulated in macrophages, accompanied by increased IL-6 (p < 0.01) and decreased TNF-α (p < 0.05) secretion. Virtual knockout linked these genes to proteostasis regulation. Although public cohort validation showed limited single-cell diagnostic capacity (AUC ≈ 0.5-0.6) requiring larger-cohort evaluation, these findings highlight key macrophage-driven molecular networks in the PCa microenvironment.
conclusionsOur analyses identify Subset 1 as a pro-inflammatory macrophage population associated with a tumor-supportive phenotype within the PCa microenvironment, with in vitro co-culture data supporting expression changes in its candidate marker genes, though comprehensive subset-signature and functional causal validation remains to be performed. Because they were identified in a macrophage subset rather than in tumor epithelium, CALU, ARID1B, and MARF1 are proposed as microenvironment-associated genes linked to this subset; their limited cell-level discriminatory capacity indicates that any biomarker potential remains preliminary and requires further patient-level evaluation in larger independent cohorts.
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