Silencing of circular RNA PUM1 inhibits clear cell renal cell carcinoma progression through the miR-340-5p/FABP7 axis.

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Receptors and Signal Transduction Pub Date : 2022-04-01 Epub Date: 2021-01-20 DOI:10.1080/10799893.2020.1870494
Fanchang Zeng, Liumei Luo, Mi Song, Daoyuan Li
{"title":"Silencing of circular RNA PUM1 inhibits clear cell renal cell carcinoma progression through the miR-340-5p/FABP7 axis.","authors":"Fanchang Zeng,&nbsp;Liumei Luo,&nbsp;Mi Song,&nbsp;Daoyuan Li","doi":"10.1080/10799893.2020.1870494","DOIUrl":null,"url":null,"abstract":"<p><p>Circular RNAs (circRNAs) monitor the development of clear cell renal cell carcinoma (ccRCC). However, the role of CircPUM1 in ccRCC malignancy is not studied. We estimated the mechanism of CircPUM1 in ccRCC progression in this study. CircPUM1 expression in ccRCC tissues and cells was detected. The expression of CircPUM1 was interfered in ccRCC cells, and its effects on the growth of ccRCC cells were studied. Nuclear/cytosol fractionation assay was performed for the location of CircPUM1, and the downstream miR, gene, and pathway involved in ccRCC progression were explored through gain- and loss-of-function experiments. CircPUM1 was highly expressed in ccRCC samples and cells. Inhibition of CircPUM1 prevented the growth ccRCC cells. CircPUM1 was localized in the cytoplasm and bound to miR-340-5p. Overexpression of miR-340-5p inhibited the growth of ccRCC cells. miR-340-5p targeted FABP7, and CircPUM1 induced FABP7 expression and the activation of MEK/ERK pathway through competitively binding to miR-340-5p. Overexpression of FABP7 attenuated the inhibitory effect of CircPUM1 silencing on the growth of ccRCC cells. Overall, CircPUM1 upregulates FABP7 expression by competitively binding to miR-340-5p, and then activates the MEK/ERK pathway, thus promoting ccRCC progression.</p>","PeriodicalId":16962,"journal":{"name":"Journal of Receptors and Signal Transduction","volume":null,"pages":null},"PeriodicalIF":2.6000,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/10799893.2020.1870494","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Receptors and Signal Transduction","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/10799893.2020.1870494","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/1/20 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 9

Abstract

Circular RNAs (circRNAs) monitor the development of clear cell renal cell carcinoma (ccRCC). However, the role of CircPUM1 in ccRCC malignancy is not studied. We estimated the mechanism of CircPUM1 in ccRCC progression in this study. CircPUM1 expression in ccRCC tissues and cells was detected. The expression of CircPUM1 was interfered in ccRCC cells, and its effects on the growth of ccRCC cells were studied. Nuclear/cytosol fractionation assay was performed for the location of CircPUM1, and the downstream miR, gene, and pathway involved in ccRCC progression were explored through gain- and loss-of-function experiments. CircPUM1 was highly expressed in ccRCC samples and cells. Inhibition of CircPUM1 prevented the growth ccRCC cells. CircPUM1 was localized in the cytoplasm and bound to miR-340-5p. Overexpression of miR-340-5p inhibited the growth of ccRCC cells. miR-340-5p targeted FABP7, and CircPUM1 induced FABP7 expression and the activation of MEK/ERK pathway through competitively binding to miR-340-5p. Overexpression of FABP7 attenuated the inhibitory effect of CircPUM1 silencing on the growth of ccRCC cells. Overall, CircPUM1 upregulates FABP7 expression by competitively binding to miR-340-5p, and then activates the MEK/ERK pathway, thus promoting ccRCC progression.

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
沉默环状RNA PUM1通过miR-340-5p/FABP7轴抑制透明细胞肾细胞癌的进展。
环状rna (circRNAs)监测透明细胞肾细胞癌(ccRCC)的发展。然而,CircPUM1在ccRCC恶性肿瘤中的作用尚未研究。我们在本研究中估计了CircPUM1在ccRCC进展中的机制。检测CircPUM1在ccRCC组织和细胞中的表达。在ccRCC细胞中干扰CircPUM1的表达,研究其对ccRCC细胞生长的影响。通过核/细胞质分离测定CircPUM1的位置,并通过功能获得和功能丧失实验探索下游miR、基因和参与ccRCC进展的途径。CircPUM1在ccRCC样品和细胞中高表达。抑制CircPUM1可抑制ccRCC细胞的生长。CircPUM1定位于细胞质中,并与miR-340-5p结合。过表达miR-340-5p可抑制ccRCC细胞的生长。miR-340-5p靶向FABP7, CircPUM1通过与miR-340-5p的竞争性结合诱导FABP7表达并激活MEK/ERK通路。过表达FABP7可减弱CircPUM1沉默对ccRCC细胞生长的抑制作用。总的来说,CircPUM1通过竞争性结合miR-340-5p上调FABP7的表达,进而激活MEK/ERK通路,从而促进ccRCC的进展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 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.
期刊最新文献
Allosteric covalent inhibition of TOE1 as potential unexplored anti-cancer target: structure-based virtual screening and covalent molecular dynamics analysis. Virtual screening, molecular docking and dynamics simulation studies to identify potential agonists of orphan receptor GPR78 targeting CNS disorders. An in-silico approach - molecular docking analysis of flavonoids against GSK-3β and TNF-α targets in Alzheimer's disease. Heat shock protein (Hsp27)-ceramide synthase (Cers1) protein-protein interactions provide a new avenue for unexplored anti-cancer mechanism and therapy. The vasodilator effect of Eugenol on uterine artery - potential therapeutic applications in pregnancy-associated hypertension.
×
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