Article(id=1291404301042185211, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404284806030089, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.04.023, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1730131200000, receivedDateStr=2024-10-29, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824378499, onlineDateStr=2026-08-04, pubDate=1740672000000, pubDateStr=2025-02-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824378499, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824378499, creator=13701087609, updateTime=1785824378499, updator=13701087609, issue=Issue{id=1291404284806030089, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='4', pageStart='451', pageEnd='600', issueExtLink='null', onlineDate='null', pubDate='1740672000000', pubDateStr='2025-02-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824374629, creator='13701087609', updateTime=1785824374629, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=561, endPage=564, ext={EN=ArticleExt(id=1291404302942204924, articleId=1291404301042185211, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Investigating the mechanism of
Dioscorea bulbifera L. against non-small cell lung cancer based on network pharmacology and molecular docking, columnId=1246531412438966969, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Reader’s Field, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the mechanism of Dioscorea bulbifera L. against non-small cell lung cancer (NSCLC) by network pharmacology and molecular docking.
Methods The active components and corresponding targets of Dioscorea bulbifera L. were retrieved by the traditional Chinese medicine systems pharmacology database and analysis platform. NSCLC targets were obtained and intersected. Protein-protein interaction (PPI) network analysis was performed using STRING database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis of intersection targets were performed. Molecular docking techniques were used to predict the binding of core components to key targets.
Results Fifteen possible active components and 203 targets of active components were screened out. There were 1 653 targets for NSCLC and 120 intersection targets. The key targets were tumor antigen p53 (TP53), RAC-alpha serine/threonine-protein kinase (AKT1), transcription factor Jun (JUN), tumor necrosis factor (TNF) and interleukin-6 (IL-6) by PPI network analysis. GO and KEGG enrichment analysis showed that the key targets were mainly in transcription regulator complex, and through response to inorganic substance, played DNA-binding transcription factor binding function, and anti-NSCLC by regulating in cancer pathways. Molecular docking results showed that diosgenin and diosbulbin B were better bound to key targets.
Conclusion The anti-NSCLC effect of Dioscorea bulbifera L. may be related to the regulation of cancer pathways by the action of diosgenin and diosbulbin B on TP53, AKT1, JUN, TNF and IL-6.
, authors=Yue CHEN, Rong JI, Zi-jun ZHANG, Yong-ze HUANG, Hong-yu BAI, Bin-bin SONG, authorsList=Yue CHEN, Rong JI, Zi-jun ZHANG, Yong-ze HUANG, Hong-yu BAI, Bin-bin SONG, authorCompany=null, correspAuthors=Bin-bin SONG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1291404303365829629, articleId=1291404301042185211, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=基于网络药理学及分子对接探讨黄药子抗非小细胞肺癌的作用机制, columnId=1246531414020219657, journalTitle=中国临床药理学杂志, columnName=读者园地, runingTitle=null, highlight=null, articleAbstract=
目的 通过网络药理学和分子对接的方法探讨黄药子抗非小细胞肺癌的作用机制。
方法 用中药系统药理学数据库与分析平台检索黄药子的活性成分及其对应靶点，经数据库获取非小细胞肺癌相关靶点，并与黄药子成分靶点取交集；用STRING数据库对交集靶点进行蛋白质互作（PPI）分析，用进行基因本体（GO）和京都基因与基因组百科全书（KEGG）富集分析，用分子对接技术推测核心成分与关键靶点的结合作用。
结果 筛选出黄药子可能有效成分15个，有效成分靶点203个；非小细胞肺癌靶点1 653个；交集靶点120个。PPI分析得到核心靶点为肿瘤蛋白P53（TP53）、丝氨酸/苏氨酸激酶1（AKT1）、转录因子Jun（JUN）、肿瘤坏死因子（TNF）和白细胞介素-6（IL-6）等。GO及KEGG富集分析显示：关键靶标主要在转录调控复合体等位置，通过调控DNA结合转录因子等功能，参与无机物的反应等生物过程，调节癌症通路等发挥抗非小细胞肺癌作用。分子对接结果表明：薯蓣皂苷元和黄毒素B与核心靶点的结合更好。
结论 黄药子抗非小细胞肺癌作用可能与薯蓣皂苷元及黄毒素B作用于TP53、AKT1、JUN、TNF和IL-6等靶点，调节癌症通路有关。
, authors=陈玥, 吉荣, 张紫珺, 黄涌泽, 白宏羽, 宋彬彬, authorsList=陈玥, 吉荣, 张紫珺, 黄涌泽, 白宏羽, 宋彬彬, authorCompany=null, correspAuthors=宋彬彬, authorNote=
陈玥（1999-），女，硕士研究生，主要从事抗肿瘤药物临床药理方面的相关研究
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