Article(id=1276976133748953418, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20250905.702, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1751904000000, receivedDateStr=2025-07-08, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384435355, onlineDateStr=2026-06-25, pubDate=1768406400000, pubDateStr=2026-01-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384435355, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384435355, creator=13701087609, updateTime=1782384435355, updator=13701087609, issue=Issue{id=1276976057215488893, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='2', pageStart='301', pageEnd='600', issueExtLink='null', onlineDate='null', pubDate='1768406400000', pubDateStr='2026-01-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1782384417107, creator='13701087609', updateTime=1782384524478, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976507658563977, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976507658563978, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=515, endPage=523, ext={EN=ArticleExt(id=1276976134327767372, articleId=1276976133748953418, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Effects and mechanisms of diosgenin on cell cycle and migration in triple-negative breast cancer MDA-MB-231 cells, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

This study aimed to elucidate the mechanisms of diosgenin, a natural compound derived from traditional Chinese medicine, on the triple-negative breast cancer cell line MDA-MB-231, with a focus on its induction of cell cycle arrest and inhibition of cell migration. Multiple experimental approaches were employed, including RNA sequencing analysis, flow cytometry for cell cycle detection, wound healing assays to evaluate migration capacity, F-actin staining to observe cytoskeletal changes, transmission electron microscopy (TEM) to examine cellular morphology and filopodia alterations, as well as Western blot and immunofluorescence staining to detect the expression of related proteins. RNA sequencing revealed significant gene expression differences between the diosgenin-treated group and the control group, with KEGG and GO analyses showing enrichment of differentially expressed genes mainly in pathways related to cell cycle and migration. Flow cytometry demonstrated that diosgenin induced G₀/G₁ phase arrest in MDA-MB-231 cells in a dose-dependent manner. Further Western blot and immunofluorescence assays indicated that diosgenin regulated the cell cycle via the CDC25A-CDK2/4/6 axis. Wound healing assays showed that diosgenin significantly inhibited cell migration. F-actin staining indicated that diosgenin suppressed F-actin formation and disrupted its structure. TEM observations revealed a reduction in filopodia formation on the cell surface after diosgenin treatment. Moreover, Western blot and immunofluorescence results demonstrated that diosgenin inhibited migration by suppressing epithelial-mesenchymal transition (EMT) and the RhoA-ROCK1 signaling pathway. In conclusion, diosgenin induces G₀/G₁ phase arrest in MDA-MB-231 cells by regulating cell cycle-related proteins and significantly inhibits cell migration by suppressing F-actin formation, reducing filopodia on the cell surface, and inhibiting EMT and the RhoA-ROCK1 pathway.

, authors=null, authorsList=Yi-rui YU, Xin WEN, Jia-rong ZHANG, Jin-hang HU, authorCompany=null, correspAuthors=Jin-hang HU, 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=1276976135112102222, articleId=1276976133748953418, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=薯蓣皂苷元对三阴性乳腺癌MDA-MB-231细胞周期与迁移的作用及机制研究, columnId=1276975994707775974, journalTitle=中国中药杂志, columnName=药理, runingTitle=null, highlight=null, articleAbstract=

该研究旨在阐明中药来源的天然产物薯蓣皂苷元对三阴性乳腺癌MDA-MB-231细胞系的作用机制，重点解析其诱导细胞周期阻滞及抑制细胞迁移的潜在分子机制。该研究综合运用多种实验方法，包括RNA测序分析，流式细胞术检测细胞周期，划痕愈伤实验评估细胞迁移能力，F-actin染色观察细胞骨架变化，透射电子显微镜观察细胞形态和伪足变化，以及Western blot和免疫荧光染色检测相关蛋白表达等。RNA测序结果显示，薯蓣皂苷元处理组与对照组之间存在显著的基因表达差异，通过KEGG和GO分析揭示差异表达基因主要富集于细胞周期和迁移相关通路。流式细胞术检测发现，薯蓣皂苷元以剂量依赖性方式诱导MDA-MB-231细胞阻滞于G₀/G₁期，进一步的Western blot和免疫荧光实验表明，薯蓣皂苷元通过调控细胞分裂周期蛋白25A（CDC25A）-细胞周期蛋白依赖性激酶（CDK）2/4/6轴影响细胞周期进程。划痕愈伤实验结果显示，薯蓣皂苷元显著抑制细胞迁移能力。F-actin染色结果显示薯蓣皂苷元可抑制F-actin生成并破坏其结构。透射电镜观察表明，薯蓣皂苷元能够减少细胞表面伪足的形成。此外，Western blot和免疫荧光实验结果表明，薯蓣皂苷元通过抑制上皮-间质转化（EMT）进程和Ras同源基因家族成员A（RhoA）-Rho关联含卷曲螺旋结合蛋白激酶1（ROCK1）信号通路，进而抑制细胞的迁移能力。综上所述，薯蓣皂苷元通过调控细胞周期相关蛋白表达诱导MDA-MB-231细胞发生G₀/G₁期阻滞，并且通过抑制F-actin生成，减少细胞表面伪足形成、抑制EMT进程及RhoA-ROCK1信号通路，显著抑制细胞的迁移能力。

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