ArticleJournal of bone oncology2025
Assessing the mechanism of osteosarcoma induced by long-term PET exposure: prediction from combined network toxicology, machine learning and molecular docking.
Article in Journal of bone oncology, 2025. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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5 authors.
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Abstract
Objective: Polyethylene terephthalate (PET) has emerged as a focal point in addressing global pollution and a critical environmental issue due to its potential health hazards. However, its role in the pathogenesis of osteosarcoma (OS) and the underlying molecular mechanisms remain largely unexplored, further highlighting the necessity of assessing its molecular toxicity. Methods: This study integrated network toxicology, machine learning, molecular docking, and CIBERSORT-based immune infiltration analysis to systematically investigate the potential impact of PET exposure on contracting OS, elucidating its biological functions, signaling mechanisms, and immune microenvironment. Molecular docking was further applied to characterize the binding properties of PET with hub proteins, and potential therapeutic agents for OS were predicted. Results: We identified 12 potential key targets of OS associated with PET exposure and, through machine learning models, selected six hub genes (i.e., BCAT1, CDK4, CSF1R, CXCR4, MYB, and PRTN3). Gene Ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) analyses were conducted to elucidate the roles of these genes in biological processes, cellular components, molecular functions, and signaling pathways. Molecular docking results revealed that PET exhibits high specificity in binding to these hub genes, particularly by interacting with CSF1R (-8.312 kcal/mol), potentially activating the PI3K-Akt signaling pathway and modulating the OS immune microenvironment to promote tumor progression through multiple mechanisms. Furthermore, drug prediction analysis identified Conclusion: This study reveals that PET may play a critical role in OS development by regulating hub genes and signaling pathways. Molecular docking analysis demonstrates that PET can tightly bind to specific target proteins, suggesting a potential molecular mechanism underlying OS progression. These findings provide a scientific basis for further evaluating PET-related health risks and offer theoretical support for the development of future prevention and treatment strategies.
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