Identification of STAT3 phosphorylation inhibitors using generative deep learning, virtual screening, molecular dynamics simulations, and biological evaluation for non-small cell lung cancer therapy

被引:1
作者
Cai, Weiji [1 ,2 ]
Jiang, Beier [3 ]
Yin, Yichen [1 ,2 ]
Ma, Lei [1 ,2 ]
Li, Tao [4 ]
Chen, Jing [1 ,2 ]
机构
[1] Ningxia Med Univ, Sch Basic Med Sci, 1160 Shengli Rd, Yinchuan 750004, Ningxia, Peoples R China
[2] Ningxia Med Univ, Key Lab Fertil Maintenance Minist Educ, Yinchuan 750004, Ningxia, Peoples R China
[3] Naval Med Univ, Navy Med Res Inst, Shanghai 200433, Peoples R China
[4] Ningxia Med Univ, Dept Oncol, Gen Hosp, Yinchuan 750004, Peoples R China
基金
中国国家自然科学基金;
关键词
NSCLC; Drug design; Signal transducer and activator of transcription 3; Molecular dynamics; Apoptosis; BINDING-AFFINITY; RESISTANCE; TARGETS; HER2;
D O I
10.1007/s11030-024-11067-5
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The development of phosphorylation-suppressing inhibitors targeting Signal Transducer and Activator of Transcription 3 (STAT3) represents a promising therapeutic strategy for non-small cell lung cancer (NSCLC). In this study, a generative model was developed using transfer learning and virtual screening, leveraging a comprehensive dataset of STAT3 inhibitors to explore the chemical space for novel candidates. This approach yielded a chemically diverse library of compounds, which were prioritized through molecular docking and molecular dynamics (MD) simulations. Among the identified candidates, the HG110 molecule demonstrated potent suppression of STAT3 phosphorylation at Tyr705 and inhibited its nuclear translocation in IL6-stimulated H441 cells. Rigorous MD simulations further confirmed the stability and interaction profiles of top candidates within the STAT3 binding site. Notably, HG106 and HG110 exhibited superior binding affinities and stable conformations, with favorable interactions involving key residues in the STAT3 binding pocket, outperforming known inhibitors. These findings underscore the potential of generative deep learning to expedite the discovery of selective STAT3 inhibitors, providing a compelling pathway for advancing NSCLC therapies.
引用
收藏
页码:3189 / 3205
页数:17
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