NEAT1/miR410-3p轴在乳腺癌细胞侵袭中的作用

IF 2.4 3区 生物学 Q2 GENETICS & HEREDITY Gene Pub Date : 2025-06-05 Epub Date: 2025-03-02 DOI:10.1016/j.gene.2025.149379
Cihangir Dogan, Ibrahim Acikbas, Buket Er Urganci, Zahra Azizi
{"title":"NEAT1/miR410-3p轴在乳腺癌细胞侵袭中的作用","authors":"Cihangir Dogan,&nbsp;Ibrahim Acikbas,&nbsp;Buket Er Urganci,&nbsp;Zahra Azizi","doi":"10.1016/j.gene.2025.149379","DOIUrl":null,"url":null,"abstract":"<div><div>Breast cancer, which is the most common cancer among women in Türkiye and throughout the world, is also one of the leading causes of cancer-related deaths. A significant factor in these deaths is metastatic breast cancer, which spreads to distant organs. The metastasis of the breast tumor follows a series of steps. Many proteins and signal molecules are in charge of these processes. In addition, NEAT1, a long noncoding RNA (lncRNA), was reported to play a key role in breast cancer cell proliferation and survival. Numerous cancer kinds were also shown to have extraordinary miR-410-3p expression levels. NEAT1 and miR-410-3p expression patterns in MCF-7 and MCF-10A cell lines were investigated using quantitative real-time polymerase chain reaction (qRT-PCR) in this study. The results demonstrated that NEAT1 was elevated by 2.30-fold in cancer cells in comparison to normal cells, whereas miR-410-3p was diminished by −2.85-fold. Furthermore, the transwell invasion experiment demonstrated the invasive potential of the MCF-7 cell line, whereas the MCF-10A cells could not invade. The target analysis revealed that functions of the targets were associated with biological adhesion and cel growth. In conclusion, a correlation was found between overexpression of NEAT1 and increased invasiveness of target cells, as well as inhibition of miR-410-3p, which is a regulatory target of NEAT1.</div></div>","PeriodicalId":12499,"journal":{"name":"Gene","volume":"951 ","pages":"Article 149379"},"PeriodicalIF":2.4000,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The role of the NEAT1/miR410-3p axis in the invasion of breast cancer cells\",\"authors\":\"Cihangir Dogan,&nbsp;Ibrahim Acikbas,&nbsp;Buket Er Urganci,&nbsp;Zahra Azizi\",\"doi\":\"10.1016/j.gene.2025.149379\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Breast cancer, which is the most common cancer among women in Türkiye and throughout the world, is also one of the leading causes of cancer-related deaths. A significant factor in these deaths is metastatic breast cancer, which spreads to distant organs. The metastasis of the breast tumor follows a series of steps. Many proteins and signal molecules are in charge of these processes. In addition, NEAT1, a long noncoding RNA (lncRNA), was reported to play a key role in breast cancer cell proliferation and survival. Numerous cancer kinds were also shown to have extraordinary miR-410-3p expression levels. NEAT1 and miR-410-3p expression patterns in MCF-7 and MCF-10A cell lines were investigated using quantitative real-time polymerase chain reaction (qRT-PCR) in this study. The results demonstrated that NEAT1 was elevated by 2.30-fold in cancer cells in comparison to normal cells, whereas miR-410-3p was diminished by −2.85-fold. Furthermore, the transwell invasion experiment demonstrated the invasive potential of the MCF-7 cell line, whereas the MCF-10A cells could not invade. The target analysis revealed that functions of the targets were associated with biological adhesion and cel growth. In conclusion, a correlation was found between overexpression of NEAT1 and increased invasiveness of target cells, as well as inhibition of miR-410-3p, which is a regulatory target of NEAT1.</div></div>\",\"PeriodicalId\":12499,\"journal\":{\"name\":\"Gene\",\"volume\":\"951 \",\"pages\":\"Article 149379\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2025-06-05\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Gene\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0378111925001672\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/3/2 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Gene","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0378111925001672","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/3/2 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
引用次数: 0

摘要

乳腺癌是日本和全世界妇女中最常见的癌症,也是导致癌症相关死亡的主要原因之一。这些死亡的一个重要因素是转移性乳腺癌,它会扩散到远处的器官。乳腺肿瘤的转移有一系列的步骤。许多蛋白质和信号分子负责这些过程。此外,NEAT1是一种长链非编码RNA (lncRNA),据报道在乳腺癌细胞增殖和存活中起关键作用。许多癌症类型也显示出异常的miR-410-3p表达水平。本研究采用实时定量聚合酶链反应(qRT-PCR)技术研究NEAT1和miR-410-3p在MCF-7和MCF-10A细胞系中的表达模式。结果表明,与正常细胞相比,NEAT1在癌细胞中升高了2.30倍,而miR-410-3p则降低了-2.85倍。此外,transwell侵袭实验表明MCF-7细胞系具有侵袭能力,而MCF-10A细胞则不具有侵袭能力。靶标分析表明,这些靶标的功能与生物粘附和细胞生长有关。综上所述,我们发现NEAT1过表达与靶细胞侵袭性增加以及NEAT1调控靶点miR-410-3p的抑制存在相关性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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
The role of the NEAT1/miR410-3p axis in the invasion of breast cancer cells
Breast cancer, which is the most common cancer among women in Türkiye and throughout the world, is also one of the leading causes of cancer-related deaths. A significant factor in these deaths is metastatic breast cancer, which spreads to distant organs. The metastasis of the breast tumor follows a series of steps. Many proteins and signal molecules are in charge of these processes. In addition, NEAT1, a long noncoding RNA (lncRNA), was reported to play a key role in breast cancer cell proliferation and survival. Numerous cancer kinds were also shown to have extraordinary miR-410-3p expression levels. NEAT1 and miR-410-3p expression patterns in MCF-7 and MCF-10A cell lines were investigated using quantitative real-time polymerase chain reaction (qRT-PCR) in this study. The results demonstrated that NEAT1 was elevated by 2.30-fold in cancer cells in comparison to normal cells, whereas miR-410-3p was diminished by −2.85-fold. Furthermore, the transwell invasion experiment demonstrated the invasive potential of the MCF-7 cell line, whereas the MCF-10A cells could not invade. The target analysis revealed that functions of the targets were associated with biological adhesion and cel growth. In conclusion, a correlation was found between overexpression of NEAT1 and increased invasiveness of target cells, as well as inhibition of miR-410-3p, which is a regulatory target of NEAT1.
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
Gene
Gene 生物-遗传学
CiteScore
6.10
自引率
2.90%
发文量
718
审稿时长
42 days
期刊介绍: Gene publishes papers that focus on the regulation, expression, function and evolution of genes in all biological contexts, including all prokaryotic and eukaryotic organisms, as well as viruses.
期刊最新文献
The NF-κB–driven inflammatory cascade in ischemic stroke: Linking DAMPs, inflammasomes, and neurovascular dysfunction Hypokalemic periodic paralysis: novel perspectives from genetic mutations to clinical management Integrative assessment of genetic diversity and population structure in palmarosa (Cymbopogon martinii var. motia) using morphological and molecular markers Establishment and characterization of an immortalized porcine gastric epithelial cell line and identification of NPC1 as a key mediator of aflatoxin B1 toxicity Time-resolved transcriptomics of FEN1 knockdown HEK293T cells identifies altered rhythmic gene expression
×
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学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
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