ArticleFrontiers in cell and developmental biology2026
Multimodal integration of pathomics and single-cell transcriptomics reveals CDC20 as a link between prostate cancer recurrence and benzo[a]pyrene-responsive phenotypes.
Article in Frontiers in cell and developmental biology, 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
Introduction: Prostate cancer recurrence reflects molecular and histological heterogeneity, yet the cellular states harboring recurrence-associated signals and their potential environmental modifiers remain incompletely understood. Methods: We integrated single-cell RNA sequencing, bulk transcriptomes with recurrence annotation, quantitative histopathology, cross-cohort survival modeling, reverse network toxicology, molecular simulation, and cellular perturbation experiments. Results: Analysis of 36,025 cells from GSE141445 identified 14,464 malignant luminal epithelial cells. Scissor identified a recurrence-associated transcriptional state enriched for adhesion, migration, angiogenesis, and proliferation programs. H&E-derived features from 304 paired TCGA-PRAD cases captured variation in this transcriptional program and supported internal recurrence risk stratification. Cross-cohort modeling prioritized CDC20, ENSA, and PTTG1. Reverse toxicology further prioritized benzo[a]pyrene (BaP), and CDC20 showed the most favorable predicted BaP docking score. In PC-3 and DU145 cells, 10 nM BaP increased CDC20 expression, whereas CDC20 silencing attenuated BaP-associated proliferation, colony formation, wound closure, and migration. Discussion: These findings identify CDC20 as a recurrence-associated molecular node involved in BaP-responsive malignant biological phenotypes and provide a phenotype-anchored framework linking recurrence biology with environmental exposure-related tumor behavior.
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