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基于网络药理学预测和分子对接的策略探索王不留行治疗结直肠癌的潜在药理作用机制

Network pharmacology prediction and molecular docking-based strategy to discover the potential pharmacological mechanism of action of Wang Bu Liu Xing () for colorectal cancer.

作者信息

Shi Yongquan, Zhang Yunshu, Liu Jifeng, Zhao Yanping, Liu Wei

机构信息

Department of Clinical Laboratory Center, Shandong Second Provincial General Hospital, Jinan, China.

Department of Traditional Medicine, First Affiliated Hospital of Dalian Medical University, Dalian, China.

出版信息

J Gastrointest Oncol. 2023 Apr 29;14(2):504-515. doi: 10.21037/jgo-23-83. Epub 2023 Apr 24.

DOI:10.21037/jgo-23-83
PMID:37201075
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10186540/
Abstract

BACKGROUND

Colorectal cancer (CRC) is the leading cause of cancer-related death worldwide. Wang Bu Liu Xing [ (SV)] is a traditional Chinese medicine (TCM) ingredient with anti-angiogenic and anti-tumor effects. However, little research has been done on the ingredients found in SV or the putative process by which SV fights CRC, and this paper aims to reveal the components of SV that are effective in treating CRC.

METHODS

The open database and online platform were used in this study, Symptom Mapping (SymMap) and Traditional Chinese Medicine Systems Pharmacology (TCMSP) for SV ingredient and targets, Gene Expression Omnibus (GEO) for differentially expressed genes (DEGs) of CRC, Database for Annotation Visualization and Integrated Discovery (DAVID) for Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, STRING-Cytoscape for protein-protein interaction (PPI), AutoDockTools for Molecular docking and others. were conducted to determine how SV affects CRC and what are the most important components, potential targets, and signaling pathways.

RESULTS

The findings of the network pharmacology study indicated that swerchirin and potential target gene for SV was connected to anti-CRC actions. SV may inhibit CRC by interacting with crucial targets like , , and . Additionally, KEGG analysis revealed that the p53 signaling pathway may be a driver of the anti-CRC impact of SV. Molecular docking showed that swerchirin can bind with its target protein in a good bond by intermolecular force.

CONCLUSIONS

In this study, the pharmacological effects of SV were examined, along with its potential therapeutic impact on CRC. These effects of SV appear to be mediated via a variety of substances, targets, and pathways. SV exerts pharmacological effects in CRC, p53 signaling pathway is great value. The main molecular docking is and swerchirin. Moreover, our research offers a promising method for characterizing therapeutic pathways and identifying molecules in TCM.

摘要

背景

结直肠癌(CRC)是全球癌症相关死亡的主要原因。王不留行(SV)是一种具有抗血管生成和抗肿瘤作用的中药成分。然而,关于SV中的成分或SV对抗CRC的假定过程的研究很少,本文旨在揭示SV中对治疗CRC有效的成分。

方法

本研究使用了开放数据库和在线平台,如用于SV成分和靶点的症状映射(SymMap)和中药系统药理学(TCMSP),用于CRC差异表达基因(DEG)的基因表达综合数据库(GEO),用于基因本体(GO)的注释可视化与整合发现数据库(DAVID)、京都基因与基因组百科全书(KEGG)富集分析,用于蛋白质-蛋白质相互作用(PPI)的STRING-Cytoscape,用于分子对接的AutoDockTools等。以确定SV如何影响CRC以及最重要的成分、潜在靶点和信号通路是什么。

结果

网络药理学研究结果表明,獐牙菜苦苷是SV的潜在靶基因,与抗CRC作用相关。SV可能通过与 、 和 等关键靶点相互作用来抑制CRC。此外,KEGG分析表明p53信号通路可能是SV抗CRC作用的驱动因素。分子对接表明獐牙菜苦苷能通过分子间力与其靶蛋白良好结合。

结论

在本研究中,研究了SV的药理作用及其对CRC的潜在治疗影响。SV的这些作用似乎是通过多种物质、靶点和途径介导的。SV在CRC中发挥药理作用,p53信号通路具有重要价值。主要的分子对接是 和獐牙菜苦苷。此外,我们的研究为表征中医治疗途径和鉴定分子提供了一种有前景的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/614a/10186540/521ec0aaf44a/jgo-14-02-504-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/614a/10186540/e2aba8dfc90b/jgo-14-02-504-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/614a/10186540/35070785f8d4/jgo-14-02-504-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/614a/10186540/bc2c70f023b6/jgo-14-02-504-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/614a/10186540/521ec0aaf44a/jgo-14-02-504-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/614a/10186540/e2aba8dfc90b/jgo-14-02-504-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/614a/10186540/35070785f8d4/jgo-14-02-504-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/614a/10186540/bc2c70f023b6/jgo-14-02-504-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/614a/10186540/521ec0aaf44a/jgo-14-02-504-f4.jpg

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