Niu Yuzhen, Pan Dabo, Shi Danfeng, Bai Qifeng, Liu Huanxiang, Yao Xiaojun
State Key Laboratory of Applied Organic Chemistry and Department of Chemistry, Lanzhou University, Lanzhou, 730000, China.
School of Pharmacy, Lanzhou University, Lanzhou, 730000, China.
PLoS One. 2015 Dec 17;10(12):e0145219. doi: 10.1371/journal.pone.0145219. eCollection 2015.
As a promising target for the treatment of lung cancer, the MutT Homolog 1 (MTH1) protein can be inhibited by crizotinib. A recent work shows that the inhibitory potency of (S)-crizotinib against MTH1 is about 20 times over that of (R)-crizotinib. But the detailed molecular mechanism remains unclear. In this study, molecular dynamics (MD) simulations and free energy calculations were used to elucidate the mechanism about the effect of chirality of crizotinib on the inhibitory activity against MTH1. The binding free energy of (S)-crizotinib predicted by the Molecular Mechanics/Generalized Born Surface Area (MM/GBSA) and Adaptive biasing force (ABF) methodologies is much lower than that of (R)-crizotinib, which is consistent with the experimental data. The analysis of the individual energy terms suggests that the van der Waals interactions are important for distinguishing the binding of (S)-crizotinib and (R)-crizotinib. The binding free energy decomposition analysis illustrated that residues Tyr7, Phe27, Phe72 and Trp117 were important for the selective binding of (S)-crizotinib to MTH1. The adaptive biasing force (ABF) method was further employed to elucidate the unbinding process of (S)-crizotinib and (R)-crizotinib from the binding pocket of MTH1. ABF simulation results suggest that the reaction coordinates of the (S)-crizotinib from the binding pocket is different from (R)-crizotinib. The results from our study can reveal the details about the effect of chirality on the inhibition activity of crizotinib to MTH1 and provide valuable information for the design of more potent inhibitors.
作为肺癌治疗的一个有前景的靶点,MutT同源蛋白1(MTH1)可被克唑替尼抑制。最近的一项研究表明,(S)-克唑替尼对MTH1的抑制效力约是(R)-克唑替尼的20倍。但具体的分子机制仍不清楚。在本研究中,我们采用分子动力学(MD)模拟和自由能计算来阐明克唑替尼的手性对其抑制MTH1活性的影响机制。通过分子力学/广义玻恩表面积(MM/GBSA)和自适应偏置力(ABF)方法预测的(S)-克唑替尼的结合自由能远低于(R)-克唑替尼,这与实验数据一致。对各个能量项的分析表明,范德华相互作用对于区分(S)-克唑替尼和(R)-克唑替尼的结合很重要。结合自由能分解分析表明,Tyr7、Phe27、Phe72和Trp117残基对于(S)-克唑替尼与MTH1的选择性结合很重要。进一步采用自适应偏置力(ABF)方法来阐明(S)-克唑替尼和(R)-克唑替尼从MTH1结合口袋中的解离过程。ABF模拟结果表明,(S)-克唑替尼从结合口袋中的反应坐标与(R)-克唑替尼不同。我们的研究结果可以揭示手性对克唑替尼抑制MTH1活性影响的细节,并为设计更有效的抑制剂提供有价值的信息。