靶向microRNA-122/CCNG1轴的长链非编码RNA CDKN2B-AS1在骨肉瘤中的刺激作用

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Abulaiti Abula, Guliayixiamu Saimaiti, Xayimardan Maimaiti, Wumitijiang Wuqikun, Alimujiang Abulaiti, Peng Ren, Aihemaitijiang Yusufu
{"title":"靶向microRNA-122/CCNG1轴的长链非编码RNA CDKN2B-AS1在骨肉瘤中的刺激作用","authors":"Abulaiti Abula,&nbsp;Guliayixiamu Saimaiti,&nbsp;Xayimardan Maimaiti,&nbsp;Wumitijiang Wuqikun,&nbsp;Alimujiang Abulaiti,&nbsp;Peng Ren,&nbsp;Aihemaitijiang Yusufu","doi":"10.1080/10799893.2020.1850784","DOIUrl":null,"url":null,"abstract":"<p><p>Osteosarcoma (OS), a prevalent aggressive malignancy in the bone, has limited therapeutic targets and diagnostic biomarkers. In the current investigation, RT-qPCR showed that CDKN2B-AS1 was enhanced in OS samples and cells. This research was set to examine the modulation of CDKN2B-AS1 in OS. The expression of CDKN2B-AS1 and downstream molecules was analyzed by RT-qPCR method. CCK8, EdU staining along with Transwell assays were applied to evaluate cell proliferation and invasion. Those <i>in vitro</i> investigations specified that silencing of CDKN2B-AS1 with shRNAs obviously impeded the proliferation and invasion of MG63 cells. To authenticate the relationships between CDKN2B-AS1 and microRNA-122-5p (miR-122-5p) or cyclin G1 (CCNG1) and miR-122-5p, we next employed luciferase reporter assay. We displayed that CDKN2B-AS1 repressed miR-122-5p to restore CCNG1 expression. All in all, our findings substantiated the indispensable function of CDKN2B-AS1 in OS progression and the possible molecular mechanism.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":"42 1","pages":"71-79"},"PeriodicalIF":2.6000,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1850784","citationCount":"5","resultStr":"{\"title\":\"The stimulative function of long noncoding RNA CDKN2B-AS1 in osteosarcoma by targeting the microRNA-122/CCNG1 axis.\",\"authors\":\"Abulaiti Abula,&nbsp;Guliayixiamu Saimaiti,&nbsp;Xayimardan Maimaiti,&nbsp;Wumitijiang Wuqikun,&nbsp;Alimujiang Abulaiti,&nbsp;Peng Ren,&nbsp;Aihemaitijiang Yusufu\",\"doi\":\"10.1080/10799893.2020.1850784\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Osteosarcoma (OS), a prevalent aggressive malignancy in the bone, has limited therapeutic targets and diagnostic biomarkers. In the current investigation, RT-qPCR showed that CDKN2B-AS1 was enhanced in OS samples and cells. This research was set to examine the modulation of CDKN2B-AS1 in OS. The expression of CDKN2B-AS1 and downstream molecules was analyzed by RT-qPCR method. CCK8, EdU staining along with Transwell assays were applied to evaluate cell proliferation and invasion. Those <i>in vitro</i> investigations specified that silencing of CDKN2B-AS1 with shRNAs obviously impeded the proliferation and invasion of MG63 cells. To authenticate the relationships between CDKN2B-AS1 and microRNA-122-5p (miR-122-5p) or cyclin G1 (CCNG1) and miR-122-5p, we next employed luciferase reporter assay. We displayed that CDKN2B-AS1 repressed miR-122-5p to restore CCNG1 expression. All in all, our findings substantiated the indispensable function of CDKN2B-AS1 in OS progression and the possible molecular mechanism.</p>\",\"PeriodicalId\":16962,\"journal\":{\"name\":\"Journal of Receptors and Signal Transduction\",\"volume\":\"42 1\",\"pages\":\"71-79\"},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2022-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/10799893.2020.1850784\",\"citationCount\":\"5\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Receptors and Signal Transduction\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1080/10799893.2020.1850784\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2020/12/6 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Receptors and Signal Transduction","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/10799893.2020.1850784","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/12/6 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 5

摘要

骨肉瘤(OS)是一种常见的骨恶性肿瘤,其治疗靶点和诊断生物标志物有限。在本研究中,RT-qPCR显示CDKN2B-AS1在OS样本和细胞中增强。本研究旨在检测CDKN2B-AS1在OS中的调制。RT-qPCR法分析CDKN2B-AS1及其下游分子的表达。CCK8、EdU染色及Transwell法检测细胞增殖及侵袭情况。这些体外研究表明,用shrna沉默CDKN2B-AS1明显阻碍了MG63细胞的增殖和侵袭。为了验证CDKN2B-AS1与microRNA-122-5p (miR-122-5p)或细胞周期蛋白G1 (CCNG1)与miR-122-5p之间的关系,我们接下来采用荧光素酶报告基因检测。我们发现CDKN2B-AS1抑制miR-122-5p以恢复CCNG1的表达。总之,我们的研究结果证实了CDKN2B-AS1在OS进展中不可或缺的功能及其可能的分子机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The stimulative function of long noncoding RNA CDKN2B-AS1 in osteosarcoma by targeting the microRNA-122/CCNG1 axis.

Osteosarcoma (OS), a prevalent aggressive malignancy in the bone, has limited therapeutic targets and diagnostic biomarkers. In the current investigation, RT-qPCR showed that CDKN2B-AS1 was enhanced in OS samples and cells. This research was set to examine the modulation of CDKN2B-AS1 in OS. The expression of CDKN2B-AS1 and downstream molecules was analyzed by RT-qPCR method. CCK8, EdU staining along with Transwell assays were applied to evaluate cell proliferation and invasion. Those in vitro investigations specified that silencing of CDKN2B-AS1 with shRNAs obviously impeded the proliferation and invasion of MG63 cells. To authenticate the relationships between CDKN2B-AS1 and microRNA-122-5p (miR-122-5p) or cyclin G1 (CCNG1) and miR-122-5p, we next employed luciferase reporter assay. We displayed that CDKN2B-AS1 repressed miR-122-5p to restore CCNG1 expression. All in all, our findings substantiated the indispensable function of CDKN2B-AS1 in OS progression and the possible molecular mechanism.

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
Journal of Receptors and Signal Transduction
Journal of Receptors and Signal Transduction 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
19
审稿时长
>12 weeks
期刊介绍: Journal of Receptors and Signal Tranduction is included in the following abstracting and indexing services: BIOBASE; Biochemistry and Biophysics Citation Index; Biological Abstracts; BIOSIS Full Coverage Shared; BIOSIS Previews; Biotechnology Abstracts; Current Contents/Life Sciences; Derwent Chimera; Derwent Drug File; EMBASE; EMBIOLOGY; Journal Citation Reports/ Science Edition; PubMed/MedLine; Science Citation Index; SciSearch; SCOPUS; SIIC.
×
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