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Mechanistic decoding of octyl methoxycinnamate-induced breast toxicity via network toxicology, mendelian
Yinghao Xiao1, Jixin Li1, Jiahui Xu1
1College of Pharmacy, Changchun University of Chinese Medicine, China.
Abstract:
Octyl methoxycinnamate (OMC), a widely used UV filter, has raised concerns due to its potential reproductive toxicity and association with endocrine disruption. This study systematically identified OMC-induced breast toxicity targets and elucidated underlying molecular mechanisms by integrating network toxicology, differential gene expression analysis, Mendelian randomization (MR), molecular docking, and molecular dynamics (MD) simulations. Using SwissTargetPrediction, OMIM, GeneCards and DisGeNET databases, 185 potential targets linked to OMC exposure and breast injury were identified. STRING and Cytoscape analyses highlighted 31 hub targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment revealed significant associations with immune responses, cell proliferation, and signaling pathways. Analysis of GEO datasets identified overlapping differentially expressed genes (DEGs) between core targets and breast cancer (BC). MR analysis demonstrated a causal relationship between PTGS2 and BC risk. Molecular docking indicated strong binding affinities between OMC and core targets, particularly MMP9. MD simulations further confirmed stable OMC-PTGS2 interactions, supporting PTGS2 as a key mediator of OMC-induced breast toxicity. This work provides a theoretical foundation for understanding OMC's breast toxicity mechanisms and lays groundwork for preventing or managing breast disorders in populations exposed to OMC-containing environments.
Insights
Octyl methoxycinnamate (OMC) may cause breast toxicity by disrupting cellular pathways. Prostaglandin-endoperoxide synthase 2 (PTGS2) is identified as a key mediator, linking OMC exposure to breast cancer risk.
Area of Science:
- Environmental Toxicology
- Molecular Biology
- Computational Biology
Background:
- Octyl methoxycinnamate (OMC) is a common UV filter with potential endocrine-disrupting and reproductive toxicity concerns.
- Understanding the molecular mechanisms of OMC-induced breast toxicity is crucial for public health.
Purpose of the Study:
- To identify molecular targets of OMC-induced breast toxicity.
- To elucidate the underlying mechanisms of OMC's effects on breast tissue.
- To investigate the link between OMC exposure and breast cancer risk.
Main Methods:
- Integrated network toxicology, differential gene expression analysis, Mendelian randomization (MR), molecular docking, and molecular dynamics (MD) simulations.
- Utilized databases like SwissTargetPrediction, OMIM, GeneCards, and DisGeNET for target identification.
- Analyzed GEO datasets and employed STRING, Cytoscape, GO, and KEGG for pathway and network analysis.
Main Results:
- Identified 185 potential OMC targets, with 31 identified as hub targets.
- Discovered significant associations with immune responses, cell proliferation, and signaling pathways.
- MR analysis revealed a causal link between PTGS2 and breast cancer risk, supported by molecular docking and MD simulations showing stable OMC-PTGS2 interactions.
Conclusions:
- Prostaglandin-endoperoxide synthase 2 (PTGS2) is a key mediator of OMC-induced breast toxicity.
- This study provides a theoretical basis for understanding OMC's adverse effects on breast health.
- Findings support the need for strategies to prevent or manage breast disorders in OMC-exposed populations.
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