Lu Hongting, Huang Pengyu, Huang Bingqi, He Dongming, Ou Xinhuai, Xu Zhanyu, Li Shikang
Department of Thoracic and Cardiovascular Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi Zhuang Autonomous Region, P. R. China.
Sci Rep. 2025 Aug 6;15(1):28781. doi: 10.1038/s41598-025-14733-2.
This study investigates the potential mechanisms by which Tris(2-butoxyethyl) phosphate (TBEP) may contribute to the development and progression of human malignancies. Fourteen representative cancer types were selected to explore the molecular pathways through which TBEP may exert its effects. By integrating network toxicology, molecular docking, and molecular dynamics (MD) simulations, we elucidated the underlying mechanisms of TBEP-related carcinogenicity. Potential targets associated with these malignancies were identified using multiple databases, including Public Chemical Database (PubChem), Search Tool for Interacting Chemicals (STITCH), SwissTargetPrediction, The Human Gene Database (GeneCards), the Online Mendelian Inheritance in Man (OMIM), and the Therapeutic Target Database (TTD). Core targets were further screened through STRING analysis and visualized using Cytoscape software. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were then performed to characterize the biological functions and pathways involved Three-dimensional structures of the core target proteins were retrieved from the Protein Data Bank (PDB), optimized using PyMOL (version 3.0.3), and subjected to molecular docking with AutoDock Vina to assess their binding affinities with TBEP. The stability of the resulting protein-ligand complexes was validated through MD simulations using GROMACS 2022. Finally, the relevance of the identified cancer types was confirmed using The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases. Overall, our findings suggest that TBEP may promote cancer development by interacting with key targets such as SRC and CASP3 and modulating critical signaling pathways. This study provides new insights into the potential carcinogenic mechanisms of TBEP and offers a theoretical foundation for future prevention and therapeutic strategies.
本研究调查了磷酸三(2-丁氧基乙基)酯(TBEP)可能促进人类恶性肿瘤发生和发展的潜在机制。选择了14种具有代表性的癌症类型,以探索TBEP可能发挥作用的分子途径。通过整合网络毒理学、分子对接和分子动力学(MD)模拟,我们阐明了TBEP相关致癌性的潜在机制。使用多个数据库,包括公共化学数据库(PubChem)、化学物质相互作用搜索工具(STITCH)、瑞士靶点预测、人类基因数据库(GeneCards)、人类孟德尔遗传在线(OMIM)和治疗靶点数据库(TTD),确定了与这些恶性肿瘤相关的潜在靶点。通过STRING分析进一步筛选核心靶点,并使用Cytoscape软件进行可视化。然后进行基因本体(GO)和京都基因与基因组百科全书(KEGG)富集分析,以表征所涉及的生物学功能和途径。从蛋白质数据库(PDB)检索核心靶蛋白的三维结构,使用PyMOL(版本3.0.3)进行优化,并与AutoDock Vina进行分子对接,以评估它们与TBEP的结合亲和力。使用GROMACS 2022通过MD模拟验证所得蛋白质-配体复合物的稳定性。最后,使用癌症基因组图谱(TCGA)和基因型-组织表达(GTEx)数据库确认所确定癌症类型的相关性。总体而言,我们的研究结果表明,TBEP可能通过与SRC和CASP3等关键靶点相互作用并调节关键信号通路来促进癌症发展。本研究为TBEP的潜在致癌机制提供了新的见解,并为未来的预防和治疗策略提供了理论基础。