LncRNA C2orf27A Promotes Gastric Cancer by Sponging MiR-610 and Elevating NOX4 Expression.

IF 3.3 3区 医学 Q2 ONCOLOGY
Journal of Cancer Pub Date : 2025-01-27 eCollection Date: 2025-01-01 DOI:10.7150/jca.100621
Mingkai Zhuang, Xiaoxiong Guo, Dan Lin, Na Lin, Xiaozhong Wang, Fenglin Chen
{"title":"LncRNA C2orf27A Promotes Gastric Cancer by Sponging MiR-610 and Elevating NOX4 Expression.","authors":"Mingkai Zhuang, Xiaoxiong Guo, Dan Lin, Na Lin, Xiaozhong Wang, Fenglin Chen","doi":"10.7150/jca.100621","DOIUrl":null,"url":null,"abstract":"<p><p>Long non-coding RNAs (lncRNAs) are crucial for gastric cancer (GC) progression. In this study, we aimed to investigate the function and molecular pathways of lncRNA C2orf27A in GC development. Bioinformatics databases, tissue cDNA microarrays, and cell lines were used to assess the expression of C2orf27A in GC. Cell proliferation was assessed using Cell Counting Kit-8, colony formation, cell cycle assays, whereas cell death using the Annexin V-APC/7-AAD assay. Subcutaneous xenograft mouse models were used to assess the effects of the C2orf27A knockdown on GC growth <i>in vivo</i>. The subcellular localization of C2orf27A in GC cells was verified using nucleocytoplasmic separation. Bioinformatics analysis predicted the binding of C2orf27A, miR-610, and NADPH oxidase 4 (NOX4), which was validated using dual luciferase reporter gene assay. We found that C2orf27A expression increased in GC tissues and cells. Furthermore, GC patients with increased C2orf27A expression levels had worse survival rates. Silencing of C2orf27A suppressed GC cell growth and induced GC cell death <i>in vitro</i> and <i>in vivo</i>. Further investigations into underlying mechanisms showed that C2orf27A functions as a competitive endogenous RNA against miR-610, leading to increased NOX4 expression levels in GC cells. Notably, blocking miR-610 and increasing NOX4 expression levels reversed the anticancer effects of reduced C2orf27A levels in GC cells. In summary, C2orf27A promotes cell proliferation and reduces cell death through the miR-610/NOX4 pathway in GC, which may provide a new perspective for further elucidation of the molecular mechanism underlying GC progression.</p>","PeriodicalId":15183,"journal":{"name":"Journal of Cancer","volume":"16 5","pages":"1504-1518"},"PeriodicalIF":3.3000,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11843226/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cancer","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.7150/jca.100621","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Long non-coding RNAs (lncRNAs) are crucial for gastric cancer (GC) progression. In this study, we aimed to investigate the function and molecular pathways of lncRNA C2orf27A in GC development. Bioinformatics databases, tissue cDNA microarrays, and cell lines were used to assess the expression of C2orf27A in GC. Cell proliferation was assessed using Cell Counting Kit-8, colony formation, cell cycle assays, whereas cell death using the Annexin V-APC/7-AAD assay. Subcutaneous xenograft mouse models were used to assess the effects of the C2orf27A knockdown on GC growth in vivo. The subcellular localization of C2orf27A in GC cells was verified using nucleocytoplasmic separation. Bioinformatics analysis predicted the binding of C2orf27A, miR-610, and NADPH oxidase 4 (NOX4), which was validated using dual luciferase reporter gene assay. We found that C2orf27A expression increased in GC tissues and cells. Furthermore, GC patients with increased C2orf27A expression levels had worse survival rates. Silencing of C2orf27A suppressed GC cell growth and induced GC cell death in vitro and in vivo. Further investigations into underlying mechanisms showed that C2orf27A functions as a competitive endogenous RNA against miR-610, leading to increased NOX4 expression levels in GC cells. Notably, blocking miR-610 and increasing NOX4 expression levels reversed the anticancer effects of reduced C2orf27A levels in GC cells. In summary, C2orf27A promotes cell proliferation and reduces cell death through the miR-610/NOX4 pathway in GC, which may provide a new perspective for further elucidation of the molecular mechanism underlying GC progression.

求助全文
约1分钟内获得全文 求助全文
来源期刊
Journal of Cancer
Journal of Cancer ONCOLOGY-
CiteScore
8.10
自引率
2.60%
发文量
333
审稿时长
12 weeks
期刊介绍: Journal of Cancer is an open access, peer-reviewed journal with broad scope covering all areas of cancer research, especially novel concepts, new methods, new regimens, new therapeutic agents, and alternative approaches for early detection and intervention of cancer. The Journal is supported by an international editorial board consisting of a distinguished team of cancer researchers. Journal of Cancer aims at rapid publication of high quality results in cancer research while maintaining rigorous peer-review process.
×
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