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首页> 外文会议>International Conference on Biosciences and Medical Engineering >Potential Role of Glyceollin as Anti-Metastatic Agent through Transforming Growth Factor-β Receptors Inhibition Signaling Pathways: A Computational Study
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Potential Role of Glyceollin as Anti-Metastatic Agent through Transforming Growth Factor-β Receptors Inhibition Signaling Pathways: A Computational Study

机译：Glyceollin作为抗转移剂通过转化生长因子-β受体抑制信号通路的潜在作用：计算研究

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Glyceollin is a phytoalexin compound derived from elicited soybean which has been proven as anti-metastatic agent through inhibition of Epithelial-Mesenchymal Transition (EMT) mechanism, but the overall mechanism remains unclear. Transforming Growth Factor-β (TGF-β) is one of the cytokines that can contribute in EMT by interacting with the TGF-β receptor (TGFBR). This study analyzed the potential of glyceollin which include glyceollin (Gln) I, II, III, and IV as TGFBR type I (TGFBR1) and II (TGFBR2) inhibitors to block signaling pathways for the EMT process. The results of binding affinity analysis through molecular docking revealed that Gln I had the potential role as TGFBR type I and II inhibitor with the smallest energy compared to other glyceollin isomers. Furthermore, Gln I had 14 and 6 interacted residues both hydrophobically and hydrogen bonded as well as a TGFBR1-inhibitor complex. Protein interaction analysis illustrated that TGFBR1 and TGFBR2 could interact with Smad-2, -3, -4, and Endoglin (ENG) which were involved in metastasis process through EMT mechanism. Augmentation of EMT regulator transcription factors activity could decrease E-cadherin expression and had implications for loss of cell-cell adhesion resulting in cancer metastasis. These data indicate that glyceollin I had a promising opportunity as an anti-metastasic compound through blockade of signaling pathways mediated by TGFBR. Further research is needed to validate glyceollin I inhibition activity in vitro against TGFBR.
机译：大豆抗毒素是从引发大豆的植物抗毒素化合物，它已被证明是抗转移剂通过抑制上皮 - 间充质转换（EMT）的机制，但总的机制尚不清楚。转化生长因子β（TGF-β）是可以通过与TGF-β受体（TGFBR）相互作用在EMT贡献的细胞因子之一。该研究分析了大豆抗毒素的，其中包括大豆抗毒素（GLN）I，II，III，和IV为TGFBR I型（TGFBR1）和II（TGFBR2）抑制剂阻断为EMT过程信号转导途径的潜力。通过分子对接结合亲和力分析的结果表明，谷氨酰胺我有潜在作用TGFBR I型和II抑制剂，具有最小的能量相对于其他大豆抗毒素异构体。此外，谷氨酰胺我有14个6相互作用残基既疏水和氢键以及一个TGFBR1 - 抑制剂复合物。蛋白质相互作用分析说明的是TGFBR1和TGFBR2可以用的Smad-2相互作用，-3，-4，并且其是通过EMT机制参与转移过程内皮糖蛋白（ENG）。 EMT调节转录因子活性的增强可以降低E-钙粘蛋白的表达和用于导致癌症转移细胞 - 细胞粘连的损失有含义。这些数据表明，大豆抗毒素我有一个有前途的机会，作为抗转移化合物，通过信令TGFBR介导的途径的封锁。需要进一步的研究来验证大豆抗毒素1抑制的体外活性针对TGFBR。

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