通过调节 miR-124/SBK1 轴抑制视网膜母细胞瘤的发展

IF 0.7 4区 材料科学 Q3 Materials Science
Qiaoling Sun, Xiaozhao Zhao, Bei Jin, Baotong Shu, Yu Ma
{"title":"通过调节 miR-124/SBK1 轴抑制视网膜母细胞瘤的发展","authors":"Qiaoling Sun, Xiaozhao Zhao, Bei Jin, Baotong Shu, Yu Ma","doi":"10.1166/mex.2023.2510","DOIUrl":null,"url":null,"abstract":"We conducted cellular and animal experiments to investigate the correlation between miR-124/SBK1 and retinoblastoma (RB) progression, as well as to elucidate the anti-cancer efficacy of chaetocin in RB. Initially, miR-124 levels showed a significant decrease in RB tissues and cells,\n which further declined with increasing tumor diameter and clinical stage. In cellular experiments, inhibiting miR-124 expression significantly enhanced the viability and invasiveness of Y79 cells, while up-regulating miR-124 suppressed the malignant biology of Y79 cells by targeting SBK1 levels,\n thereby reducing their viability and invasiveness. Subsequent animal experiments provided further evidence that SBK1 was the functional target of miR-124, and its up-regulation significantly facilitated RB progression. Additionally, chaetocin demonstrated anti-tumor effects through the upregulation\n of miR-124 and downregulation of SBK1. Therefore, chaetocin can effectively inhibit RB progression by targeting the upregulation of miR-124 and downregulation of SBK1.","PeriodicalId":18318,"journal":{"name":"Materials Express","volume":" 45","pages":""},"PeriodicalIF":0.7000,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Inhibition of chaetocin on retinoblastoma progression by modulating the miR-124/SBK1 axis\",\"authors\":\"Qiaoling Sun, Xiaozhao Zhao, Bei Jin, Baotong Shu, Yu Ma\",\"doi\":\"10.1166/mex.2023.2510\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"We conducted cellular and animal experiments to investigate the correlation between miR-124/SBK1 and retinoblastoma (RB) progression, as well as to elucidate the anti-cancer efficacy of chaetocin in RB. Initially, miR-124 levels showed a significant decrease in RB tissues and cells,\\n which further declined with increasing tumor diameter and clinical stage. In cellular experiments, inhibiting miR-124 expression significantly enhanced the viability and invasiveness of Y79 cells, while up-regulating miR-124 suppressed the malignant biology of Y79 cells by targeting SBK1 levels,\\n thereby reducing their viability and invasiveness. Subsequent animal experiments provided further evidence that SBK1 was the functional target of miR-124, and its up-regulation significantly facilitated RB progression. Additionally, chaetocin demonstrated anti-tumor effects through the upregulation\\n of miR-124 and downregulation of SBK1. Therefore, chaetocin can effectively inhibit RB progression by targeting the upregulation of miR-124 and downregulation of SBK1.\",\"PeriodicalId\":18318,\"journal\":{\"name\":\"Materials Express\",\"volume\":\" 45\",\"pages\":\"\"},\"PeriodicalIF\":0.7000,\"publicationDate\":\"2023-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Materials Express\",\"FirstCategoryId\":\"88\",\"ListUrlMain\":\"https://doi.org/10.1166/mex.2023.2510\",\"RegionNum\":4,\"RegionCategory\":\"材料科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Materials Science\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Materials Express","FirstCategoryId":"88","ListUrlMain":"https://doi.org/10.1166/mex.2023.2510","RegionNum":4,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Materials Science","Score":null,"Total":0}
引用次数: 0

摘要

我们通过细胞和动物实验研究miR-124/SBK1与视网膜母细胞瘤(retinoblastoma, RB)进展的相关性,并阐明缩宫素对RB的抗癌作用。最初,miR-124水平在RB组织和细胞中显著降低,随着肿瘤直径和临床分期的增加,miR-124水平进一步下降。在细胞实验中,抑制miR-124的表达可显著增强Y79细胞的活力和侵袭性,而上调miR-124可通过靶向SBK1水平抑制Y79细胞的恶性生物学,从而降低其活力和侵袭性。随后的动物实验进一步证明,SBK1是miR-124的功能靶点,其上调可显著促进RB的进展。此外,催产素通过上调miR-124和下调SBK1显示出抗肿瘤作用。因此,催产素可以通过靶向miR-124的上调和SBK1的下调,有效抑制RB进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Inhibition of chaetocin on retinoblastoma progression by modulating the miR-124/SBK1 axis
We conducted cellular and animal experiments to investigate the correlation between miR-124/SBK1 and retinoblastoma (RB) progression, as well as to elucidate the anti-cancer efficacy of chaetocin in RB. Initially, miR-124 levels showed a significant decrease in RB tissues and cells, which further declined with increasing tumor diameter and clinical stage. In cellular experiments, inhibiting miR-124 expression significantly enhanced the viability and invasiveness of Y79 cells, while up-regulating miR-124 suppressed the malignant biology of Y79 cells by targeting SBK1 levels, thereby reducing their viability and invasiveness. Subsequent animal experiments provided further evidence that SBK1 was the functional target of miR-124, and its up-regulation significantly facilitated RB progression. Additionally, chaetocin demonstrated anti-tumor effects through the upregulation of miR-124 and downregulation of SBK1. Therefore, chaetocin can effectively inhibit RB progression by targeting the upregulation of miR-124 and downregulation of SBK1.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Materials Express
Materials Express NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
自引率
0.00%
发文量
69
审稿时长
>12 weeks
期刊介绍: Information not localized
×
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