Paeoniflorin inhibits colorectal cancer cell stemness through the miR-3194-5p/catenin beta-interacting protein 1 axis.

IF 2.7 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL Kaohsiung Journal of Medical Sciences Pub Date : 2023-10-01 Epub Date: 2023-08-02 DOI:10.1002/kjm2.12736
Zhao Su, Beier Hu, Jing Li, Zhichun Zeng, Hu Chen, Yuhang Guo, Yun Mao, Wen Cao
{"title":"Paeoniflorin inhibits colorectal cancer cell stemness through the miR-3194-5p/catenin beta-interacting protein 1 axis.","authors":"Zhao Su,&nbsp;Beier Hu,&nbsp;Jing Li,&nbsp;Zhichun Zeng,&nbsp;Hu Chen,&nbsp;Yuhang Guo,&nbsp;Yun Mao,&nbsp;Wen Cao","doi":"10.1002/kjm2.12736","DOIUrl":null,"url":null,"abstract":"<p><p>Paeoniflorin (PF) is a natural plant ingredient with remarkable antitumor effects. Herein, we investigated the biological effects and mechanism of PF in colorectal cancer (CRC) cell stemness. The messenger RNA (mRNA) and protein expressions were assessed using quantitative real-time polymerase chain reaction and western blot. The viability, proliferation, and migration and invasion of CRC cells were evaluated using cell counting kit-8, clone-formation, and transwell migration and invasion assays, respectively. The sphere-formation capacity was determined using the sphere-formation assay. A dual-luciferase reporter gene assay was employed to analyze the interaction between miR-3194-5p and catenin beta-interacting protein 1 (CTNNBIP1). The viability, migration, invasion, epithelial-mesenchymal transition, and stemness of CRC cells were repressed by PF. MiR-3194-5p was upregulated in CRC tissues and cells. MiR-3194-5p knockdown suppressed CRC cell stemness, while miR-3194-5p overexpression had the opposite effect. In addition, the inhibition of CRC cell stemness caused by PF was eliminated by miR-3194-5p overexpression. CTNNBIP1 functioned as the target of miR-3194-5p, whose knockdown abrogated the repression of CRC cell stemness and Wnt/β-catenin signaling activation by PF.PF regulated the miR-3194-5p/CTNNBIP1/Wnt/β-catenin axis to repress CRC cell stemness.</p>","PeriodicalId":49946,"journal":{"name":"Kaohsiung Journal of Medical Sciences","volume":null,"pages":null},"PeriodicalIF":2.7000,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Kaohsiung Journal of Medical Sciences","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1002/kjm2.12736","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/8/2 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

Abstract

Paeoniflorin (PF) is a natural plant ingredient with remarkable antitumor effects. Herein, we investigated the biological effects and mechanism of PF in colorectal cancer (CRC) cell stemness. The messenger RNA (mRNA) and protein expressions were assessed using quantitative real-time polymerase chain reaction and western blot. The viability, proliferation, and migration and invasion of CRC cells were evaluated using cell counting kit-8, clone-formation, and transwell migration and invasion assays, respectively. The sphere-formation capacity was determined using the sphere-formation assay. A dual-luciferase reporter gene assay was employed to analyze the interaction between miR-3194-5p and catenin beta-interacting protein 1 (CTNNBIP1). The viability, migration, invasion, epithelial-mesenchymal transition, and stemness of CRC cells were repressed by PF. MiR-3194-5p was upregulated in CRC tissues and cells. MiR-3194-5p knockdown suppressed CRC cell stemness, while miR-3194-5p overexpression had the opposite effect. In addition, the inhibition of CRC cell stemness caused by PF was eliminated by miR-3194-5p overexpression. CTNNBIP1 functioned as the target of miR-3194-5p, whose knockdown abrogated the repression of CRC cell stemness and Wnt/β-catenin signaling activation by PF.PF regulated the miR-3194-5p/CTNNBIP1/Wnt/β-catenin axis to repress CRC cell stemness.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
芍药苷通过miR-3194-5p/连环蛋白β相互作用蛋白1轴抑制癌症细胞干细胞。
芍药苷是一种具有显著抗肿瘤作用的天然植物成分。在此,我们研究了PF在结直肠癌癌症(CRC)细胞干燥中的生物学效应和机制。信使核糖核酸(信使核糖核酸)和蛋白质表达采用实时定量聚合酶链反应和蛋白质印迹法进行评估。分别使用细胞计数试剂盒-8、克隆形成和transwell迁移和入侵测定来评估CRC细胞的生存能力、增殖以及迁移和入侵。使用球体形成测定法测定球体形成能力。采用双荧光素酶报告基因测定法分析miR-3194-5p和连环蛋白-β相互作用蛋白1(CTNNBIP1)之间的相互作用。PF抑制CRC细胞的活力、迁移、侵袭、上皮-间质转化和干性。MiR-3194-5p在CRC组织和细胞中上调。MiR-3194-5p敲低抑制CRC细胞的干性,而MiR-3194-5p过表达具有相反的作用。此外,miR-3194-5p过表达消除了PF对CRC细胞干性的抑制。CTNNBIP1作为miR-3194-5p的靶标,其敲除消除了PF.PF对CRC细胞干性和Wnt/β-catenin信号激活的抑制。PF调节miR-3194-56/CTNBIP1/Wnt/β-连环蛋白轴以抑制CRC细胞干性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Kaohsiung Journal of Medical Sciences
Kaohsiung Journal of Medical Sciences 医学-医学:研究与实验
CiteScore
5.60
自引率
3.00%
发文量
139
审稿时长
4-8 weeks
期刊介绍: Kaohsiung Journal of Medical Sciences (KJMS), is the official peer-reviewed open access publication of Kaohsiung Medical University, Taiwan. The journal was launched in 1985 to promote clinical and scientific research in the medical sciences in Taiwan, and to disseminate this research to the international community. It is published monthly by Wiley. KJMS aims to publish original research and review papers in all fields of medicine and related disciplines that are of topical interest to the medical profession. Authors are welcome to submit Perspectives, reviews, original articles, short communications, Correspondence and letters to the editor for consideration.
期刊最新文献
Retraction: Hong Liu, Shi-Ying Ren, Yan Qu, Cui Liu, Yi Zhang, Xiang Qing Li, Hong Ma. MiR-194-5p inhibited metastasis and EMT of nephroblastoma cells through targeting Crk. The Kaohsiung Journal of Medical Sciences, Volume 36, Issue 4 Apr 2020. Pages 265-273. https://doi.org/10.1002/kjm2.12180. Analysis of macular choroidal thickness in normal Taiwanese eyes by enhanced depth imaging optical coherence tomography. Bloodletting acupuncture on venules between BL60 and BL61 rapidly relieving a 4-month episode of low back pain. Mechanism of DYRK1a in myocardial ischemia-reperfusion injury by regulating ferroptosis of cardiomyocytes. Silenced LASP1 interacts with DNMT1 to promote TJP2 expression and attenuate articular cartilage injury in mice by suppressing TJP2 methylation.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1