Article(id=1309634620967186637, tenantId=1146029695717560320, journalId=1227999776411738115, issueId=1309634614356968036, articleNumber=null, orderNo=null, doi=10.12048/j.issn.1674-229X.2026.03.006, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1760889600000, receivedDateStr=2025-10-20, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1790170825473, onlineDateStr=2026-09-23, pubDate=1774368000000, pubDateStr=2026-03-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1790170825473, onlineIssueDateStr=2026-09-23, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1790170825473, creator=13701087609, updateTime=1790170825473, updator=13701087609, issue=Issue{id=1309634614356968036, tenantId=1146029695717560320, journalId=1227999776411738115, year='2026', volume='36', issue='3', pageStart='161', pageEnd='240', issueExtLink='null', onlineDate='null', pubDate='1774368000000', pubDateStr='2026-03-25', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1790170823897, creator='13701087609', updateTime=1790219059643, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1309836929789682362, tenantId=1146029695717560320, journalId=1227999776411738115, issueId=1309634614356968036, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1309836929789682363, tenantId=1146029695717560320, journalId=1227999776411738115, issueId=1309634614356968036, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=191, endPage=198, ext={EN=ArticleExt(id=1309634622598770894, articleId=1309634620967186637, tenantId=1146029695717560320, journalId=1227999776411738115, language=EN, title=Exploring the Mechanism of Danthron in Suppressing Breast Cancer Proliferation Based on Transcriptomics and Network Pharmacology, columnId=null, journalTitle=Pharmacy Today, columnName=null, runingTitle=null, highlight=null, articleAbstract=
OBJECTIVE To screen and identify the potential targets and pathways of Danthron against breast cancer based on network pharmacology, and to verify its mechanisms through transcriptomic analysis and in vitro and in vivo experiments.
METHODS Multiple databases were integrated to screen the common targets of Danthron and breast cancer for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. CCK-8 and colony formation assays were used to evaluate cell proliferation. Transcriptome sequencing and quantitative real-time polymerase chain reaction (qPCR) were performed to analyze the expression of Cxcl10, Isg15, IL-6, Nlrp3, and Bax and other related genes. A mouse 4T1 xenograft model was established to observe and assess the antitumor effect of Danthron.
RESULTS A total of 84 intersecting targets were obtained, mainly enriched in the Apoptosis, p53, PI3K-Akt, NOD-like receptor, and Cytokine signaling pathways. Danthron significantly inhibited breast cancer cell proliferation (IC50=30.05 μmol·L‐1), upregulated interferon-stimulated genes (Irf7, Isg15, Ifit1) and chemokines (Cxcl10, IL‐6), and upregulated the expression of Nlrp3 and Bax. In vivo, Danthron significantly suppressed 4T1 xenograft growth and reduced Ki-67 expression.
CONCLUSION Danthron exerts antitumor activity against breast cancer by activating interferon responses and inflammation-apoptosis-related pathways, providing a theoretical basis for its development as a potential natural anticancer agent.
, authors=Guanglian LIN, Chen ZHU
*, authorsList=Guanglian LIN, Chen ZHU, authorCompany=null, correspAuthors=Chen ZHU, 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=1309634622938509519, articleId=1309634620967186637, tenantId=1146029695717560320, journalId=1227999776411738115, language=CN, title=基于转录组学和网络药理学探讨丹蒽醌抑制乳腺癌增殖的作用机制, columnId=1228268589086606089, journalTitle=今日药学, columnName=论著, runingTitle=null, highlight=null, articleAbstract=
目的 基于网络药理学筛选丹蒽醌（Danthron）抗乳腺癌的潜在靶点及通路，并结合转录组及体内外实验验证其机制。
方法 整合多数据库筛选丹蒽醌与乳腺癌共同靶点，进行GO、KEGG分析；采用CCK-8、克隆形成实验检测细胞增殖；通过转录组及qPCR分析Cxcl10、Isg15、IL-6、Nlrp3、Bax等基因表达；建立小鼠4T1移植瘤模型观察抗肿瘤作用。
结果 共得84个交集靶点，主要富集于Apoptosis、p53、PI3K-Akt、NOD-like receptor及Cytokine信号通路。丹蒽醌显著抑制乳腺癌细胞增殖（IC50=30.05 μmol·L‐1），上调干扰素刺激基因（Irf7、Isg15、Ifit1）及趋化因子Cxcl10、IL-6，并促进Nlrp3、Bax表达。动物实验显示丹蒽醌明显抑制移植瘤生长并降低Ki-67表达。
结论 丹蒽醌通过激活干扰素应答及炎症-凋亡相关通路抑制乳腺癌细胞生长，为其作为潜在天然抗肿瘤药物提供理论依据。
, authors=林广炼, 朱晨
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