Long Noncoding RNA CRNDE Promotes Gastric Cancer Progression through Targeting miR-136-5p/MIEN1.

IF 2.4 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL Cancer Biotherapy and Radiopharmaceuticals Pub Date : 2024-12-01 Epub Date: 2024-07-04 DOI:10.1089/cbr.2023.0179
Yingchao Gu, Chaoyu Li, Xiankun Ren, Xiaodong Hu, Yuwen Huang, Lin Xia
{"title":"Long Noncoding RNA CRNDE Promotes Gastric Cancer Progression through Targeting miR-136-5p/MIEN1.","authors":"Yingchao Gu, Chaoyu Li, Xiankun Ren, Xiaodong Hu, Yuwen Huang, Lin Xia","doi":"10.1089/cbr.2023.0179","DOIUrl":null,"url":null,"abstract":"<p><p><b><i>Background:</i></b> Long noncoding RNAs (lncRNAs) contribute to the initiation and progression of gastric cancer (GC). This study examined the potential role of lncRNA colorectal neoplasia differentially expressed (CRNDE) in modulating the expression of migration and invasion enhancer 1 (MIEN1) through the suppression of miR-136-5p in GC. <b><i>Methods:</i></b> The biological roles of CRNDE, miR-136-5p, and MIEN1 in GC were assessed both in laboratory settings and through the examination of clinical samples. <b><i>Results:</i></b> CRNDE was found to be significantly increased in GC tissues, and this upregulation was associated with an unfavorable prognosis of GC patients. <i>In vitro</i> experiments showed that inhibiting cell growth and migration, along with promoting apoptosis in GC cells, could be achieved by either disabling CRNDE or MIEN1, or by increasing the expression of miR-136-5p. MIEN1 is a specific recipient of miR-136-5p, and the anticancer effects of miR-136-5p can be counteracted by the increased expression of MIEN1. Through the examination of clinical specimens, it has been observed that there is a significant positive correlation between the expression of MIEN1 and CRNDE. In contrast, miR-136-5p expression in GC tissues shows a negative correlation. <b><i>Conclusion:</i></b> A previously unexplored therapeutic target for GC involves the CRNDE/miR-136-5p/MIEN1 signal transduction cascade.</p>","PeriodicalId":55277,"journal":{"name":"Cancer Biotherapy and Radiopharmaceuticals","volume":" ","pages":"770-781"},"PeriodicalIF":2.4000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Biotherapy and Radiopharmaceuticals","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1089/cbr.2023.0179","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/7/4 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Long noncoding RNAs (lncRNAs) contribute to the initiation and progression of gastric cancer (GC). This study examined the potential role of lncRNA colorectal neoplasia differentially expressed (CRNDE) in modulating the expression of migration and invasion enhancer 1 (MIEN1) through the suppression of miR-136-5p in GC. Methods: The biological roles of CRNDE, miR-136-5p, and MIEN1 in GC were assessed both in laboratory settings and through the examination of clinical samples. Results: CRNDE was found to be significantly increased in GC tissues, and this upregulation was associated with an unfavorable prognosis of GC patients. In vitro experiments showed that inhibiting cell growth and migration, along with promoting apoptosis in GC cells, could be achieved by either disabling CRNDE or MIEN1, or by increasing the expression of miR-136-5p. MIEN1 is a specific recipient of miR-136-5p, and the anticancer effects of miR-136-5p can be counteracted by the increased expression of MIEN1. Through the examination of clinical specimens, it has been observed that there is a significant positive correlation between the expression of MIEN1 and CRNDE. In contrast, miR-136-5p expression in GC tissues shows a negative correlation. Conclusion: A previously unexplored therapeutic target for GC involves the CRNDE/miR-136-5p/MIEN1 signal transduction cascade.

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 CRNDE 通过靶向 miR-136-5p/MIEN1 促进胃癌进展
背景:长非编码RNA(lncRNA)有助于胃癌(GC)的发生和发展。本研究旨在探讨 lncRNA 大肠癌差异表达(CRNDE)通过抑制 miR-136-5p 在 GC 中调节迁移和侵袭增强子 1(MIEN1)表达的潜在作用。研究方法通过实验室环境和临床样本检查评估了 CRNDE、miR-136-5p 和 MIEN1 在胃癌中的生物学作用。结果研究发现 CRNDE 在 GC 组织中明显增高,这种上调与 GC 患者的不良预后有关。体外实验表明,抑制细胞生长和迁移以及促进 GC 细胞凋亡可以通过禁用 CRNDE 或 MIEN1 或增加 miR-136-5p 的表达来实现。MIEN1 是 miR-136-5p 的特异性受体,miR-136-5p 的抗癌作用可被 MIEN1 的表达增加所抵消。通过对临床标本的研究发现,MIEN1 的表达与 CRNDE 之间存在显著的正相关性。相比之下,miR-136-5p 在 GC 组织中的表达呈负相关。结论以前尚未探索的 GC 治疗靶点涉及 CRNDE/miR-136-5p/MIEN1 信号转导级联。
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
7.80
自引率
2.90%
发文量
87
审稿时长
3 months
期刊介绍: Cancer Biotherapy and Radiopharmaceuticals is the established peer-reviewed journal, with over 25 years of cutting-edge content on innovative therapeutic investigations to ultimately improve cancer management. It is the only journal with the specific focus of cancer biotherapy and is inclusive of monoclonal antibodies, cytokine therapy, cancer gene therapy, cell-based therapies, and other forms of immunotherapies. The Journal includes extensive reporting on advancements in radioimmunotherapy, and the use of radiopharmaceuticals and radiolabeled peptides for the development of new cancer treatments.
期刊最新文献
EIF4A3-Induced hsa_circ_0118578 Expression Enhances the Tumorigenesis of Papillary Thyroid Cancer. GRHPR, Targeted by miR-138-5p, Inhibits the Proliferation and Metastasis of Hepatocellular Carcinoma Through PI3K/AKT Signaling Pathway. Hsa_Circ_002144 Promotes Glycolysis and Immune Escape of Breast Cancer Through miR-326/PKM Axis. Long Noncoding RNA CRNDE Promotes Gastric Cancer Progression through Targeting miR-136-5p/MIEN1. Human Biodistribution and Radiation Dosimetry of the Targeting Fibroblast Growth Factor Receptor 1-Positive Tumors Tracer [68Ga]Ga-DOTA-FGFR1-Peptide.
×
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