Long-Noncoding RNA (lncRNA) EGOT Prevents the Malignant Process of Colorectal Carcinoma by Regulating BTG3

IF 2.9 4区 医学 Q1 Medicine Journal of biomedical nanotechnology Pub Date : 2024-04-01 DOI:10.1166/jbn.2024.3823
Zhengdong Wang, Dezhi Gu, Aiming Zhou
{"title":"Long-Noncoding RNA (lncRNA) EGOT Prevents the Malignant Process of Colorectal Carcinoma by Regulating BTG3","authors":"Zhengdong Wang, Dezhi Gu, Aiming Zhou","doi":"10.1166/jbn.2024.3823","DOIUrl":null,"url":null,"abstract":"This study investigates the role of the long non-coding RNA EGOT in colorectal cancer (CRC) by examining its expression in 40 pairs of CRC and adjacent normal tissues and assessing its impact on clinical outcomes. EGOT was found to be downregulated in CRC tissues, and low EGOT levels\n were associated with a higher likelihood of lymphatic and distant metastasis, as well as poorer overall and progression-free survival in CRC patients. Functional experiments revealed that overexpression of EGOT in SW480 cells reduced cell viability, migration, and wound closure, while knockdown\n of EGOT in LoVo cells had the opposite effect. In vivo experiments with nude mice confirmed that EGOT downregulation accelerated CRC growth, whereas its overexpression slowed tumor growth. The study identified BTG3 as the target gene of EGOT, and they exhibited a negative correlation\n in CRC tissues. Rescue experiments demonstrated that BTG3 could reverse the effects of EGOT on CRC cell phenotypes. In conclusion, EGOT is a downregulated molecule in CRC, closely associated with metastasis and patient prognosis. It exerts a suppressive influence on CRC cell proliferation,\n migration, and tumorigenesis by negatively regulating BTG3.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9000,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biomedical nanotechnology","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1166/jbn.2024.3823","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0

Abstract

This study investigates the role of the long non-coding RNA EGOT in colorectal cancer (CRC) by examining its expression in 40 pairs of CRC and adjacent normal tissues and assessing its impact on clinical outcomes. EGOT was found to be downregulated in CRC tissues, and low EGOT levels were associated with a higher likelihood of lymphatic and distant metastasis, as well as poorer overall and progression-free survival in CRC patients. Functional experiments revealed that overexpression of EGOT in SW480 cells reduced cell viability, migration, and wound closure, while knockdown of EGOT in LoVo cells had the opposite effect. In vivo experiments with nude mice confirmed that EGOT downregulation accelerated CRC growth, whereas its overexpression slowed tumor growth. The study identified BTG3 as the target gene of EGOT, and they exhibited a negative correlation in CRC tissues. Rescue experiments demonstrated that BTG3 could reverse the effects of EGOT on CRC cell phenotypes. In conclusion, EGOT is a downregulated molecule in CRC, closely associated with metastasis and patient prognosis. It exerts a suppressive influence on CRC cell proliferation, migration, and tumorigenesis by negatively regulating BTG3.
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
长非编码 RNA(lncRNA)EGOT 通过调控 BTG3 防止结直肠癌的恶性过程
这项研究通过检测长非编码RNA EGOT在40对结肠直肠癌(CRC)和邻近正常组织中的表达,并评估其对临床结果的影响,从而研究长非编码RNA EGOT在结肠直肠癌(CRC)中的作用。研究发现,EGOT在CRC组织中被下调,EGOT水平低与CRC患者淋巴转移和远处转移的可能性较高以及总生存期和无进展生存期较差有关。功能实验显示,在 SW480 细胞中过表达 EGOT 会降低细胞活力、迁移和伤口闭合,而在 LoVo 细胞中敲除 EGOT 则会产生相反的效果。裸鼠体内实验证实,下调 EGOT 会加速 CRC 的生长,而过表达则会减缓肿瘤的生长。研究发现 BTG3 是 EGOT 的靶基因,两者在 CRC 组织中呈负相关。拯救实验表明,BTG3 可以逆转 EGOT 对 CRC 细胞表型的影响。总之,EGOT 是一种在 CRC 中下调的分子,与转移和患者预后密切相关。它通过负调控 BTG3 对 CRC 细胞的增殖、迁移和肿瘤发生产生抑制作用。
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
CiteScore
4.30
自引率
17.20%
发文量
145
审稿时长
2.3 months
期刊介绍: Information not localized
期刊最新文献
Mechanism of miR-126 Loaded in Albumin Nanoparticles for Reversing the Multidrug Resistance in Breast Carcinoma Cells Application of 20(S)-Protopanaxadiol-Loaded Nanostructured Lipid Carriers for Diabetic Wound Healing and Vascular Regeneration LncRNA NEAT1 Promotes the Cancer Stem Cell-Like Properties of HCC by miR-128-3p/GP73 Axis Pterostilbene-Loaded Polydopamine Nanoparticles Down-Regulate Tumor Necrosis Factor-α and Improve Myocardial Function in Mice with Acute Myocardial Infarction Phacoemulsification Plus Intraocular Lens Implantation with Gold Nanoparticles for Complicated Cataract Secondary to Uveitis: Efficacy Analysis
×
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