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CA1-Associated Epithelial-State Remodeling in Colon Cancer Cells Exposed to Polystyrene Nanoplastics: Integrated Multi-Omics and In Vitro Analyses.
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Researchers studied human colon cancer cells and lab-grown organoids exposed to polystyrene nanoplastics, using gene analysis and computer modeling. Exposure lowered levels of a protein called CA1 and related genes, along with changes linked to inflammation and cell stress, and increased wound-closure activity in colon cancer cells grown in dishes.
Polystyrene nanoplastics (PS-NPs) directly encounter the gastrointestinal epithelium after ingestion, yet the epithelial molecular states linking exposure to colon cancer cell behavior remain unclear. We integrated bulk transcriptomics, interpretable machine learning, WGCNA, single-cell and spatial transcriptomics, structural analyses, and in vitro experiments to investigate CA1-associated epithelial responses. Intersecting 2,139 colon cancer differentially expressed genes with 766 styrene-associated genes yielded 159 candidates. Among 45 classification models, LASSO+GBM ranked highest in an exploratory cross-cohort comparison, with an apparent training AUC of 1.000 and comparison-cohort AUCs of 0.999 and 0.925. CA1 had the highest SHAP importance and was located in the WGCNA module most strongly associated with tumor/normal status. Single-cell and organoid analyses showed attenuation of epithelial CA1/CA2 and carbonic anhydrase-bicarbonate-related programs, with concordant spatial trends; TCGA-COAD and Human Protein Atlas data further supported reduced CA1 expression. Low CA1 was associated with reduced metabolic and bicarbonate-related programs and enhanced inflammatory signaling. Docking and 100 ns molecular dynamics showed only weak, dynamic styrene-CA1 contacts. In HCT116 cells, PS-NPs decreased CA1, CA2, and Occludin expression, altered stress-, inflammation-, and apoptosis-related molecules, and increased scratch closure, with generally stronger changes at higher doses and after Tioxolone co-treatment. Collectively, these findings identify a CA1/CA2-low epithelial state associated with PS-NP exposure and suggest that CA1-associated epithelial-state remodeling may be part of the cellular response to PS-NPs.
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