ArticleBMC pharmacology & toxicology2026
Integrative bioinformatics, network toxicology, and molecular docking elucidate molecular mechanisms of ATBC-induced sarcoma progression with experimental validation.
Article in BMC pharmacology & toxicology, 2026. 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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Abstract
backgroundAcetyl tributyl citrate (ATBC), a widely used plasticizer, has raised health concerns due to its potential environmental persistence and human exposure, but its toxicological effects on sarcoma remain unclear.
methodsWe employed an integrated approach combining network toxicology, molecular docking, survival analysis, and experimental validation to systematically investigate ATBC’s impact on sarcoma.
resultsMulti-database screening identified 102 overlapping targets. Protein–protein interaction analysis revealed six hub genes: TLR4, ESR1, PPARG, SIRT1, NFKB1, and PTGS2. Functional enrichment analysis indicated significant involvement in cancer-related pathways, including PI3K–Akt, HIF‑1, and AGE–RAGE signaling. Molecular docking predicted potential interactions between ATBC and these targets, with binding energies ranging from -1.15 to -2.99 kcal/mol. Survival analysis associated high PPARG expression with poor prognosis, while high TLR4 and ESR1 expression correlated with better survival. In vitro experiments showed ATBC promoted proliferation and migration of sarcoma cells. qPCR results confirmed ATBC downregulated TLR4 and ESR1 and upregulated PPARG, aligning with clinical prognostic trends.
conclusionsThese findings suggest ATBC may exert tumor-promoting effects by modulating core targets and pathways, highlighting its potential role in sarcoma progression and the importance of environmental health risk assessment.
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