Investigating the effects of air pollution on papillary thyroid cancer based on network toxicology and molecular docking.
[BACKGROUND] Recent studies have highlighted the association between various diseases and air pollution.
APA
Chen Z, Yang Y, et al. (2026). Investigating the effects of air pollution on papillary thyroid cancer based on network toxicology and molecular docking.. Discover oncology, 17(1), 296. https://doi.org/10.1007/s12672-026-04450-1
MLA
Chen Z, et al.. "Investigating the effects of air pollution on papillary thyroid cancer based on network toxicology and molecular docking.." Discover oncology, vol. 17, no. 1, 2026, pp. 296.
PMID
41548183
Abstract
[BACKGROUND] Recent studies have highlighted the association between various diseases and air pollution. This study aims to investigate the impact of air pollutants on the pathogenesis of papillary thyroid carcinoma (PTC) and the underlying molecular mechanisms, as well as to identify key genes involved in this process.
[METHODS] Datasets related to air pollutants and PTC were sourced from multiple databases. Differentially expressed genes in PTC were identified using weighted gene co-expression network analysis (WGCNA). Protein–protein interaction (PPI) analysis and visualization of intersecting genes were performed. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to explore potential mechanisms. Finally, molecular docking analysis was performed to examine the interactions between key genes and air pollutants.
[RESULTS] Eleven common air pollutants (SO, toluene, benzene, CO, NO, NO, O, di-n-octyl acetate, di-n-octyl phthalate, Hg, and Pb) were selected. Three cross-target genes associated with PTC were identified: CYP3A4, DRD2, and CYP2C9. GO/KEGG enrichment analysis suggested that air pollution may induce PTC through chemical carcinogenesis and drug metabolism pathways. Further analysis using STRING and Cytoscape software identified 23 core targets. Additionally, molecular docking experiments confirmed a strong binding affinity and stable complex formation between CYP2C9 and dioctyl phthalate.
[CONCLUSION] This study, integrating network toxicology and molecular docking, identified three shared targets (CYP3A4, DRD2, and CYP2C9) and several enriched pathways linking common air pollutants to the molecular mechanisms of PTC. These findings provide valuable hypotheses and highlight candidate genes and pathways for future mechanistic and epidemiological studies on air pollution-related thyroid carcinogenesis, though causal relationships have not been established.
[SUPPLEMENTARY INFORMATION] The online version contains supplementary material available at 10.1007/s12672-026-04450-1.
[METHODS] Datasets related to air pollutants and PTC were sourced from multiple databases. Differentially expressed genes in PTC were identified using weighted gene co-expression network analysis (WGCNA). Protein–protein interaction (PPI) analysis and visualization of intersecting genes were performed. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted to explore potential mechanisms. Finally, molecular docking analysis was performed to examine the interactions between key genes and air pollutants.
[RESULTS] Eleven common air pollutants (SO, toluene, benzene, CO, NO, NO, O, di-n-octyl acetate, di-n-octyl phthalate, Hg, and Pb) were selected. Three cross-target genes associated with PTC were identified: CYP3A4, DRD2, and CYP2C9. GO/KEGG enrichment analysis suggested that air pollution may induce PTC through chemical carcinogenesis and drug metabolism pathways. Further analysis using STRING and Cytoscape software identified 23 core targets. Additionally, molecular docking experiments confirmed a strong binding affinity and stable complex formation between CYP2C9 and dioctyl phthalate.
[CONCLUSION] This study, integrating network toxicology and molecular docking, identified three shared targets (CYP3A4, DRD2, and CYP2C9) and several enriched pathways linking common air pollutants to the molecular mechanisms of PTC. These findings provide valuable hypotheses and highlight candidate genes and pathways for future mechanistic and epidemiological studies on air pollution-related thyroid carcinogenesis, though causal relationships have not been established.
[SUPPLEMENTARY INFORMATION] The online version contains supplementary material available at 10.1007/s12672-026-04450-1.
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