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分子对接和分子动力学研究揭示了抑制剂表没食子儿茶素没食子酸酯(EGCG)和OSU-03012对胶质母细胞瘤中过表达的葡萄糖调节蛋白78(GRP78)的抑制作用和选择性的结构基础。

Molecular docking and molecular dynamics studies reveal structural basis of inhibition and selectivity of inhibitors EGCG and OSU-03012 toward glucose regulated protein-78 (GRP78) overexpressed in glioblastoma.

作者信息

Bhattacharjee Rituparna, Devi Arpita, Mishra Seema

机构信息

Department of Biochemistry, School of Life Sciences, University of Hyderabad, Hyderabad, 500046, India.

出版信息

J Mol Model. 2015 Oct;21(10):272. doi: 10.1007/s00894-015-2801-3. Epub 2015 Sep 29.

Abstract

Glioblastoma (GBM), a malignant form of brain tumor, has a high mortality rate. GRP78, one of the HSP70 protein family members, is overexpressed in GBM. GRP78 is the key chaperone protein involved in the unfolded protein response. Upregulated GRP78 expression in cancer cells inhibits apoptosis and promotes chemoresistance. GRP78 has an ATPase domain, a substrate-binding domain, and a linker region. ATP-competitive inhibitors such as EGCG and OSU-03012 inhibit GRP78 activity and reduce its expression in GBM. However, there is a lack of structural data on the binding modes of these inhibitors to GRP78 ATPase domain. Further, the mode of selectivity of these inhibitors toward GRP78 also is unknown. Toward this end, molecular docking was performed with AutoDock Vina and confirmation obtained by docking using ROSIE. The stability and MM-PBSA binding energy of GRP78-inhibitor complexes as well as energetic contribution of individual residues was analyzed by 50 ns molecular dynamics run with GROMACS. MSA by ClustalW2 identified unique amino acid residues in the ATPase domain of GRP78 which were different from the residues present in other HSP70 proteins. Important and unique amino acid residues of GRP78 such as Ile61, Glu293, Arg297, and Arg367 played a major role in the intermolecular interactions with these inhibitors. The interactions with unique residues of GRP78 as compared with those of HSP70-1A provided the basis for selectivity. It was found that the binding affinity and specificity/selectivity of EGCG toward GRP78 was higher than that toward HSP70-1A, and selectivity was even better than OSU-03012. OSU-03012 was predicted to bind to GRP78. Analyses from MD runs showed tight binding and stability of complexes, and the highest number of hydrogen bonds during the trajectory runs were comparable to those found in the docking studies. Energetic contribution of individual inhibitor-interacting residues showed that energy values of Ile61 and Glu293 were among the most negative. These studies are, to the best of our knowledge, the first studies characterizing EGCG and OSU-03012 interactions with GRP78 on a structural basis and provide a significant insight into their binding modes, selectivity, and structural stability.

摘要

胶质母细胞瘤(GBM)是一种恶性脑肿瘤,死亡率很高。GRP78是热休克蛋白70(HSP70)家族成员之一,在GBM中过表达。GRP78是未折叠蛋白反应中关键的伴侣蛋白。癌细胞中GRP78表达上调会抑制细胞凋亡并促进化疗耐药性。GRP78具有一个ATP酶结构域、一个底物结合结构域和一个连接区。表没食子儿茶素没食子酸酯(EGCG)和OSU-03012等ATP竞争性抑制剂可抑制GRP78活性并降低其在GBM中的表达。然而,关于这些抑制剂与GRP78 ATP酶结构域结合模式的结构数据尚缺。此外,这些抑制剂对GRP78的选择性模式也不清楚。为此,使用AutoDock Vina进行分子对接,并通过ROSIE对接获得确认。使用GROMACS进行50纳秒的分子动力学模拟,分析GRP78-抑制剂复合物的稳定性和MM-PBSA结合能以及各个残基的能量贡献。通过ClustalW2进行的多序列比对(MSA)确定了GRP78 ATP酶结构域中独特的氨基酸残基,这些残基与其他HSP70蛋白中的残基不同。GRP78的重要且独特的氨基酸残基,如异亮氨酸61、谷氨酸293、精氨酸297和精氨酸367,在与这些抑制剂的分子间相互作用中起主要作用。与HSP70-1A相比,与GRP78独特残基的相互作用为选择性提供了基础。研究发现,EGCG对GRP78的结合亲和力和特异性/选择性高于对HSP70-1A的,且选择性甚至优于OSU-03012。预测OSU-03012会与GRP78结合。分子动力学模拟分析表明复合物结合紧密且稳定,轨迹模拟过程中氢键数量最多,与对接研究中的结果相当。各个与抑制剂相互作用残基的能量贡献表明,异亮氨酸61和谷氨酸293的能量值是最负的之一。据我们所知,这些研究是首次在结构基础上表征EGCG和OSU-03012与GRP78相互作用的研究,为它们的结合模式、选择性和结构稳定性提供了重要见解。

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