Article(id=1291404913762882377, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404791758975909, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.11.009, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1733241600000, receivedDateStr=2024-12-04, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824524584, onlineDateStr=2026-08-04, pubDate=1750089600000, pubDateStr=2025-06-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824524584, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824524584, creator=13701087609, updateTime=1785824524584, updator=13701087609, issue=Issue{id=1291404791758975909, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='11', pageStart='1501', pageEnd='1650', issueExtLink='null', onlineDate='null', pubDate='1750089600000', pubDateStr='2025-06-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824495496, creator='13701087609', updateTime=1785824495496, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=1544, endPage=1549, ext={EN=ArticleExt(id=1291404913964208970, articleId=1291404913762882377, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of plantamajoside on the growth and metastasis of non-small cell lung cancer, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the regulatory mechanism of plantamajoside (PMS) on the growth and metastasis of non-small cell lung cancer (NSCLC).
Methods A549 cells were divided into control group (normal culture), model group (40 μg·mL-1 PMS), NC inhibitor group (40 μg·mL-1 PMS+NC inhibitor), miR-525-5p inhibitor group (40 μg·mL-1 PMS+miR-525-5p inhibitor), sh-NC group (40 μg·mL-1 PMS+miR-525-5p inhibitor+sh-NC) and sh-ubiquitin conjugating enzyme E2C (UBE2C) group (40 μg·mL-1 PMS+miR-525-5p inhibitor+sh-UBE2C). Transwell assay was used to evaluate the invasion ability of A549 cells after different treatments. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay was used to evaluate the apoptosis of A549 cells after different treatments. At the animal level, mice were injected with A549 cell suspension (5×106/100 μL) to construct the NSCLC model. They were randomly divided into model-M group, PMS group (50 mg·kg-1 PMS), miR-525-5p inhibitor-M group (50 mg·kg-1 PMS+miR-525-5p inhibitor) and sh-UBE2C-M group (50 mg·kg-1 PMS+miR-525-5p inhibitor+sh-UBE2C). All groups were treated for 5 days with once a day. The size of the transplanted tumor was measured with a ruler every 7 days, and the transplanted tumor was removed and weighed on the 28th day. The number of Transwell invasions in control group, model group, NC inhibitor group, miR-525-5p inhibitor group, sh-NC group and sh-UBE2C group were 173.62±23.46, 82.05±14.17, 84.69±13.82, 143.48±19.81, 139.57±18.24 and 105.93±16.25, respectively; the apoptosis rates were (22.65±4.01)%, (53.34±8.93)%, (51.46±8.81)%, (37.52±5.86)%, (34.83±5.27)% and (48.75±6.19)%, respectively. Compared in model group and control group, compared in miR-525-5p inhibitor group and NC inhibitor group, compared in sh-UBE2C group and sh-NC group, there were significant differences in the number of Transwell invasion and apoptosis rates (all P<0.05). At the animal level, 28 d tumor volumes of model-M group, PMS group, miR-525-5p inhibitor-M group and sh-UBE2C-M group were (966.30±176.53), (495.70±52.40), (841.10±121.25) and (623.80±105.85) mm3, respectively; the tumor weight on day 28 were (1.43±0.52), (0.75±0.21), (1.32±0.43) and (0.85±0.26) g, respectively. Differences of the tumor volume and weight between PMS group and model-M group, sh-UBE2C-M group and miR-525-5p inhibitor-M group were statistically significant at the 28th day (P<0.01, P<0.001).
Conclusion PMS can significantly inhibit the growth and metastasis of NSCLC by regulating the miR-525-5p/UBE2C axis.
, authors=He-ping ZHU
1a, Ming YE
1a, Qun CHEN
1a, Ming-bao ZHA
1b, authorsList=He-ping ZHU, Ming YE, Qun CHEN, Ming-bao ZHA, authorCompany=null, correspAuthors=Ming-bao ZHA, 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=1291404914492691275, articleId=1291404913762882377, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=车前子苷抑制非小细胞肺癌生长和转移的研究, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 探讨车前子苷（PMS）影响非小细胞肺癌（NSCLC）生长和转移的调控机制。
方法 将A549细胞分为对照组（正常培养）、实验组（40 μg·mL-1 PMS）、NC inhibitor组（40 μg·mL-1 PMS+NC inhibitor）、miR-525-5p inhibitor组（40 μg·mL-1 PMS+miR-525-5p inhibitor）、sh-NC组（40 μg·mL-1 PMS+miR-525-5p inhibitor+sh-NC）、sh-泛素结合酶E2C（UBE2C）组（40 μg·mL-1 PMS+miR-525-5p inhibitor+sh-UBE2C）。用穿透小室实验检测细胞的侵袭能力；用原位末端转移酶标记法检测细胞凋亡情况。将小鼠注射A549细胞悬液（5×106/100 μL）以构建NSCLC模型，随机分为动物模型组、PMS组（50 mg·kg-1 PMS）、动物miR-525-5p inhibitor组（50 mg·kg-1 PMS+miR-525-5p inhibitor）、动物sh-UBE2C组（50 mg·kg-1 PMS+miR-525-5p inhibitor+sh-UBE2C），均每天给药1次，连续给药5 d。每7 d用直尺测量各组小鼠移植瘤的体积大小，第28天取出移植瘤并称质量。
结果 对照组、实验组、NC inhibitor组、miR-525-5p inhibitor组、sh-NC组和sh-UBE2C组的Transwell侵袭数目分别为（173.62±23.46）、（82.05±14.17）、（84.69±13.82）、（143.48±19.81）、（139.57±18.24）和（105.93±16.25）个，细胞凋亡率分别为（22.65±4.01）%、（53.34±8.93）%、（51.46±8.81）%、（37.52±5.86）%、（34.83±5.27）%和（48.75±6.19）%，实验组的上述指标与对照组比较、miR-525-5p inhibitor组的上述指标与NC inhibitor组比较、sh-UBE2C组的上述指标与sh-NC组比较，在统计学上差异均有统计学意义（均P<0.05）。在动物水平上，动物模型组、PMS组、动物miR-525-5p inhibitor组和动物sh-UBE2C组第28天肿瘤体积分别为（966.30±176.53）、（495.70±52.40）、（841.10±121.25）和（623.80±105.85）mm3，第28天肿瘤质量分别为（1.43±0.52）、（0.75±0.21）、（1.32±0.43）和（0.85±0.26）g，PMS组的上述指标与动物模型组比较，动物sh-UBE2C组的上述指标与动物miR-525-5p inhibitor组比较，在统计学上差异均有统计学意义（P<0.01，P<0.001）。
结论 PMS能通过调控miR-525-5p/UBE2C轴显著抑制NSCLC的生长和转移。
, authors=朱和平
1a, 叶鸣
1a, 陈群
1a, 查名宝
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朱和平（1980-），男，副主任药师，主要从事药物研究方面的工作
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