Multi-omics analysis of perfluorooctanoic acid and glioblastoma: insights from Mendelian randomization, network toxicology, and molecular docking - PubMed
5 hours ago
- #Environmental Carcinogens
- #Multi-omics Integration
- #Brain Tumors
- Genetic predisposition to higher circulating levels of perfluorooctanoic acid (PFOA) is causally linked to an increased risk of glioblastoma, as shown by Mendelian randomization analysis.
- Network toxicology identified 86 overlapping molecular targets between PFOA and glioblastoma, with nine hub genes including IL1B, MYC, BCL2, ALB, EGFR, ESR1, IL6, TNF, and CASP3.
- Key biological pathways implicated include AGE-RAGE signaling, response to xenobiotic stimuli, chemical carcinogenesis-receptor activation, and positive regulation of glial cell proliferation.
- Molecular docking predicts strong binding interactions between PFOA and all hub proteins, with the highest affinities for MYC and TNF, suggesting direct mechanistic involvement.
- Cisplatin was identified as a top candidate for drug repositioning based on interaction analysis, offering potential therapeutic opportunities for glioblastoma linked to PFOA exposure.