TYMSOS-miR-101-3p-NETO2 axis promotes osteosarcoma progression

IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS
Zun Zhang , Jin Wang , Xiaoyan Zhang , Bo Ran , Jie Wen , Hong Zhang
{"title":"TYMSOS-miR-101-3p-NETO2 axis promotes osteosarcoma progression","authors":"Zun Zhang ,&nbsp;Jin Wang ,&nbsp;Xiaoyan Zhang ,&nbsp;Bo Ran ,&nbsp;Jie Wen ,&nbsp;Hong Zhang","doi":"10.1016/j.mcp.2022.101887","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Osteosarcoma (OS) is a type of bone cancer most often affects pre-teens and teens, but it is still a rare disorder. Neuropilin and tolloid-like 2 (NETO2) has been reported to promote OS progression, but its upstream mechanism in OS cells remains obscure.</p></div><div><h3>Methods</h3><p>Quantitative real-time PCR (RT-qPCR) and Western blot were conducted to examine RNA and protein levels, separately. Functional assays were performed to assess the impact of NETO2 on OS cell malignancy. Moreover, bioinformatics analyses and mechanism experiments were performed to identify the upstream mechanism of NETO2 in OS cells.</p></div><div><h3>Results</h3><p>Functionally, NETO2 depletion repressed cell proliferation, migration and invasion as well as epithelial-mesenchymal transition (EMT) but triggered the apoptosis of OS cells. NETO2 is directly targeted and negatively regulated by microRNA-101-3p (miR-101-3p). Mechanically, miR-101-3p could combine with long noncoding RNA (lncRNA) TYMS opposite strand RNA (TYMSOS) in OS cells. In addition, our study proved that TYMSOS promotes the malignancy of OS via elevating NETO2 expression as miR-101-3p sponge.</p></div><div><h3>Conclusion</h3><p>TYMSOS-miR-101-3p-NETO2 axis promotes the malignant behaviors of OS cells, which might offer a novel sight for OS treatment.</p></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":null,"pages":null},"PeriodicalIF":2.3000,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular and Cellular Probes","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0890850822000986","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMICAL RESEARCH METHODS","Score":null,"Total":0}
引用次数: 3

Abstract

Background

Osteosarcoma (OS) is a type of bone cancer most often affects pre-teens and teens, but it is still a rare disorder. Neuropilin and tolloid-like 2 (NETO2) has been reported to promote OS progression, but its upstream mechanism in OS cells remains obscure.

Methods

Quantitative real-time PCR (RT-qPCR) and Western blot were conducted to examine RNA and protein levels, separately. Functional assays were performed to assess the impact of NETO2 on OS cell malignancy. Moreover, bioinformatics analyses and mechanism experiments were performed to identify the upstream mechanism of NETO2 in OS cells.

Results

Functionally, NETO2 depletion repressed cell proliferation, migration and invasion as well as epithelial-mesenchymal transition (EMT) but triggered the apoptosis of OS cells. NETO2 is directly targeted and negatively regulated by microRNA-101-3p (miR-101-3p). Mechanically, miR-101-3p could combine with long noncoding RNA (lncRNA) TYMS opposite strand RNA (TYMSOS) in OS cells. In addition, our study proved that TYMSOS promotes the malignancy of OS via elevating NETO2 expression as miR-101-3p sponge.

Conclusion

TYMSOS-miR-101-3p-NETO2 axis promotes the malignant behaviors of OS cells, which might offer a novel sight for OS treatment.

TYMSOS-miR-101-3p-NETO2轴促进骨肉瘤进展
背景骨肉瘤(OS)是一种骨癌症,最常影响青少年,但它仍然是一种罕见的疾病。据报道,Neuropilin和tolloid样2(NETO2)可促进OS的进展,但其在OS细胞中的上游机制尚不清楚。方法采用实时定量聚合酶链式反应(RT-qPCR)和蛋白质印迹法分别检测RNA和蛋白质水平。进行功能测定以评估NETO2对OS细胞恶性肿瘤的影响。此外,还进行了生物信息学分析和机制实验,以确定NETO2在OS细胞中的上游机制。结果在功能上,NETO2耗竭抑制了OS细胞的增殖、迁移和侵袭以及上皮-间质转化(EMT),但引发了OS细胞凋亡。NETO2被微小RNA-101-3p(miR-101-3p)直接靶向并负调控。从机制上讲,miR-101-3p可以与OS细胞中的长非编码RNA(lncRNA)TYMS反链RNA(TYMSOS)结合。此外,我们的研究证明,TYMSOS通过提高NETO2作为miR-101-3p海绵的表达来促进OS的恶性。结论TYMSOS-miR-101-3p-NETO2轴可促进OS细胞的恶性行为,为OS的治疗提供了新的思路。
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
Molecular and Cellular Probes
Molecular and Cellular Probes 生物-生化研究方法
CiteScore
6.80
自引率
0.00%
发文量
52
审稿时长
16 days
期刊介绍: MCP - Advancing biology through–omics and bioinformatic technologies wants to capture outcomes from the current revolution in molecular technologies and sciences. The journal has broadened its scope and embraces any high quality research papers, reviews and opinions in areas including, but not limited to, molecular biology, cell biology, biochemistry, immunology, physiology, epidemiology, ecology, virology, microbiology, parasitology, genetics, evolutionary biology, genomics (including metagenomics), bioinformatics, proteomics, metabolomics, glycomics, and lipidomics. Submissions with a technology-driven focus on understanding normal biological or disease processes as well as conceptual advances and paradigm shifts are particularly encouraged. The Editors welcome fundamental or applied research areas; pre-submission enquiries about advanced draft manuscripts are welcomed. Top quality research and manuscripts will be fast-tracked.
×
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