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Hypothesis-generating network toxicology analysis of potential molecular convergence between a polystyrene oligomer proxy and papillary thyroid carcinoma
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Using computer models and public gene databases, researchers looked for overlap between targets linked to a polystyrene-related chemical structure and genes altered in papillary thyroid cancer, using patient tissue samples and gene databases. Three genes, BCL2, BAX, and FN1, showed consistent patterns in cancer samples. The study does not show that plastic exposure causes thyroid cancer in people.
Background Polystyrene microplastics (PS-MPs) are emerging environmental contaminants with endocrine-disrupting and pro-inflammatory effects, but whether PS-MPs-associated molecular targets converge with papillary thyroid carcinoma (PTC) alterations remains unclear. This hypothesis-generating study aimed to identify candidate molecular networks and cellular contexts shared between a simplified polystyrene computational proxy and PTC. Methods Putative targets from CTD and from TargetNet/SwissTargetPrediction using a five-styrene-unit oligomer proxy were intersected with thyroid cancer-related genes from OMIM and GeneCards. Protein functional-association and enrichment analyses were followed by differential expression analysis in GSE33630 (45 normal and 49 PTC samples). LASSO and SVM-RFE identified core genes; stability was examined by repeated nested resampling conditional on the seven-gene candidate panel. Individual-gene tumor-normal discrimination was assessed in GSE33630 and GSE60542. Protein patterns were evaluated qualitatively in the Human Protein Atlas and preliminarily in 15 matched PTC-adjacent tissue pairs. CIBERSORT-estimated immune fractions and two single-cell datasets were analyzed as exploratory context. Results Among 144 putative proxy-associated targets and 2,139 thyroid cancer-related genes, 75 were shared. Seven candidates overlapped with 1,306 PTC differentially expressed genes, and BCL2, BAX, and FN1 were selected by both feature-selection methods and remained stable across the tested GeneCards thresholds and CTD-only sensitivity analysis. BCL2 was downregulated, whereas BAX and FN1 were upregulated in PTC; individual-gene AUCs were 0.963, 0.941, and 0.965 in GSE33630 and 0.942, 0.907, and 0.955 in GSE60542. HPA images and clinical IHC supported the same protein-level directions. After multiple-testing correction, only the CIBERSORT-estimated neutrophil fraction differed between groups (higher in PTC; q=0.0021). Single-cell analysis localized the three genes across epithelial, stromal, and immune compartments. Conclusion BCL2, BAX, and FN1 are candidate molecular nodes at the convergence of polystyrene-proxy annotations and PTC-associated alterations. The findings do not demonstrate patient PS-MPs exposure, intact-particle effects, or causality, and require validation in material-characterized exposure experiments and exposure-aware clinical studies.
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