ArticleFrontiers in medicine2025
Analysis of the effects of acetyl tributyl citrate on bone cancer based on network toxicology and molecular docking.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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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Who cites it
2 citing papers in PubMed.
- Aspartame may promote erectile dysfunction via DPP4-mediated endothelial dysfunction and apoptosis: evidence from network toxicology, molecular dynamics simulation, and experimental validation.Frontiers in nutrition · 2026Article
- Analyzing the cytotoxicity and pro-tumorigenic role of acetyl tributyl citrate in prostate through network toxicology and the immune microenvironment.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acetyl tributyl citrate (ATBC) is a widely used environmental plasticizer that has raised concerns regarding its potential health effects, particularly its role in cancer development. Although ATBC is generally considered to have a safer profile compared to traditional phthalate-based plasticizers, research on its association with bone cancer remains limited. The aim of this study is to elucidate the complex effects of Acetyl tributyl citrate (ATBC) on bone cancer and to unravel the potential molecular mechanisms by which environmental pollutants influence the disease process. Methods: This study utilized multiple online databases to identify target genes associated with ATBC and bone cancer. Initially, protein-protein interaction (PPI) analysis and visualization of the intersecting genes were performed. Subsequently, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analyses were conducted to explore the underlying mechanisms connecting the two conditions. Finally, molecular docking was employed to validate the interactions between these compounds and their respective targets. Results: Using the CHEMBL, SwissTarget Prediction, and TargetNet databases, we screened 193 genes associated with ATBC. Additionally, we identified 4,439 genes related to bone cancer through the GeneCards, OMIM, and TTD databases, resulting in 73 intersecting genes. After rigorous refinement utilizing the STRING platform and Cytoscape software, we identified five core targets: STAT3, EGFR, MMP9, MAPK1, and MMP2. Functional enrichment analysis indicated that the core targets of ATBC's influence on bone cancer are primarily involved in the regulation of apoptosis, carcinogenesis, and cellular proliferation, among other biological processes. Finally, molecular docking simulations conducted with AutoDock confirmed robust binding interactions between ATBC and these core targets, thereby enhancing our understanding of their interactions. Conclusion: This study underscores the potential carcinogenic effects of ATBC in bone cancer, identifying key targets such as STAT3, EGFR, MMP9, MAPK1, and MMP2. The findings indicate that ATBC may facilitate the progression of bone cancer by targeting essential signaling pathways and remodeling the tumor microenvironment. This emphasizes the necessity for further research into the environmental risks associated with this plasticizer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.