Downregulated miR-100 Result in High Expression Levels of Chemokine (CXC Motif) Receptor 7 That Predict Recurrence of Lung Cancer

IF 0.1 4区 医学
Liu-Jie Gao, Ting-Ting Shao, Wan-Zhen Zheng, Jiguo Ding, Jun Li
{"title":"Downregulated miR-100 Result in High Expression Levels of Chemokine (CXC Motif) Receptor 7 That Predict Recurrence of Lung Cancer","authors":"Liu-Jie Gao, Ting-Ting Shao, Wan-Zhen Zheng, Jiguo Ding, Jun Li","doi":"10.1166/jbt.2023.2619","DOIUrl":null,"url":null,"abstract":"MicroRNAs (miRs) have been proved to play significant role in both the tumorigenesis and recurrence of lung cancer (LA). However, the identification of which miR participated in the recurrence of LA, as well as the underlying mechanism are poorly understood. Here in our article, quantitative\n analysis of the miR-100 expression in non-recurrent and recurrent LA tissues using real-time PCR (RT-qPCR) revealed that, compared to non-recurrent LA, the expression of miR-100 was significantly downregulated in recurrent ones. Especially, the chemokine (CXC motif) receptor 7 (CXCR7) level\n was negatively correlated with the expression of miR-100 in both non-recurrent and recurrent LA cell lines derived from corresponding LA tissues. The following in vitro experiments also confirmed that either miR-100 overexpression or CXCR7 depletion decreased proliferation of recurrent\n LA cells. In conclusion, miR-100 may act as a recurrence suppressor in LA through the regulation of CXCR7 expression, which might be a promising target for the prevention of LA recurrence.","PeriodicalId":15300,"journal":{"name":"Journal of Biomaterials and Tissue Engineering","volume":" ","pages":""},"PeriodicalIF":0.1000,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biomaterials and Tissue Engineering","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1166/jbt.2023.2619","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

MicroRNAs (miRs) have been proved to play significant role in both the tumorigenesis and recurrence of lung cancer (LA). However, the identification of which miR participated in the recurrence of LA, as well as the underlying mechanism are poorly understood. Here in our article, quantitative analysis of the miR-100 expression in non-recurrent and recurrent LA tissues using real-time PCR (RT-qPCR) revealed that, compared to non-recurrent LA, the expression of miR-100 was significantly downregulated in recurrent ones. Especially, the chemokine (CXC motif) receptor 7 (CXCR7) level was negatively correlated with the expression of miR-100 in both non-recurrent and recurrent LA cell lines derived from corresponding LA tissues. The following in vitro experiments also confirmed that either miR-100 overexpression or CXCR7 depletion decreased proliferation of recurrent LA cells. In conclusion, miR-100 may act as a recurrence suppressor in LA through the regulation of CXCR7 expression, which might be a promising target for the prevention of LA recurrence.
下调miR-100导致趋化因子(CXC Motif)受体7高表达,预测肺癌复发
微小RNA(miRs)已被证明在癌症(LA)的肿瘤发生和复发中起着重要作用。然而,对哪些miR参与LA复发的鉴定以及潜在机制知之甚少。在我们的文章中,使用实时PCR(RT-qPCR)对miR-100在非复发性和复发性LA组织中的表达进行定量分析,结果显示,与非复发性LA相比,miR-100在复发性LA中的表达显著下调。特别是,在衍生自相应LA组织的非复发性和复发性LA细胞系中,趋化因子(CXC基序)受体7(CXCR7)水平与miR-100的表达呈负相关。以下体外实验也证实miR-100过表达或CXCR7缺失降低了复发性LA细胞的增殖。总之,miR-100可能通过调节CXCR7的表达,作为LA的复发抑制剂,这可能是预防LA复发的一个有前途的靶点。
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 求助全文
来源期刊
自引率
0.00%
发文量
332
审稿时长
>12 weeks
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信