ArticleCurrent issues in molecular biology2026
Multiscale Transcriptomic and Molecular Modeling Analyses Suggest DCPMU-Associated Epithelial Remodeling and Tumor Microenvironment Perturbation in Prostate Cancer.
Article in Current issues in molecular 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
DCPMU, a major demethylated metabolite of diuron, is an environmentally persistent contaminant with potential endocrine-disrupting and carcinogenic relevance, yet its mechanistic association with prostate cancer remains unclear. This study investigated DCPMU-related mechanisms in prostate cancer by integrating network toxicology, molecular modeling, bulk transcriptomics, single-cell and spatial transcriptomics, and virtual perturbation analysis. Differentially expressed genes from TCGA-PRAD were intersected with DCPMU-associated and prostate cancer-related targets. Functional enrichment, machine learning screening, and external GEO validation identified seven candidate hub genes: APOBEC3G, SCGB1A1, PTGS1, CA12, CES1, FOLH1, and NOS1. Molecular docking showed favorable DCPMU binding to these proteins, and molecular dynamics simulations further supported stable interactions with PTGS1, CA12, CES1, and FOLH1. Single-cell analysis of GSE141445 revealed cell-type-specific expression, with FOLH1 and CA12 enriched in epithelial cells, CES1 in fibroblasts, and PTGS1 in mast cells. Spatial transcriptomics from GSE181294 showed tumor-enriched FOLH1 expression and increased Core4 module activity in malignant regions. Virtual knockout analysis suggested that FOLH1 perturbation was associated with predicted downstream transcriptional changes, with PTGS1 showing marked perturbation responsiveness. Overall, our integrative analyses suggest that DCPMU exposure is associated with epithelial malignancy, inflammatory metabolism, xenobiotic handling, and tumor-microenvironment remodeling, particularly within malignant epithelial niches. These hypothesis-generating findings require experimental validation to establish any causal role in prostate cancer progression.
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