Long intergenic noncoding RNA for IGF2BP2 stability suppresses gastric cancer cell apoptosis by inhibiting the maturation of microRNA-34a.

IF 1.7 4区 医学 Q2 MEDICINE, GENERAL & INTERNAL Open Medicine Pub Date : 2024-09-27 eCollection Date: 2024-01-01 DOI:10.1515/med-2024-0992
Yao Wang, Zhigang Guo, Zhifeng Yang, Qingyan Deng, Yueming Huang, Yanhong Chen
{"title":"Long intergenic noncoding RNA for IGF2BP2 stability suppresses gastric cancer cell apoptosis by inhibiting the maturation of microRNA-34a.","authors":"Yao Wang, Zhigang Guo, Zhifeng Yang, Qingyan Deng, Yueming Huang, Yanhong Chen","doi":"10.1515/med-2024-0992","DOIUrl":null,"url":null,"abstract":"<p><p>The oncogenic role of long intergenic noncoding RNA for IGF2BP2 stability (LINRIS) has been reported in colorectal cancer. This research aimed to study its potential involvement in gastric cancer (GC). In this study, paired GC and non-tumor tissues were obtained from 64 GC patients, and the levels of LINRIS, mature microRNA-34a (miR-34a), and miR-34a precursor in these tissues were measured with RT-qPCR. Linear regression was used to analyze their correlations. The role of LINRIS overexpression and siRNA silencing in regulating the maturation of miR-34a was analyzed by RT-qPCR. Cell apoptosis was studied with flow cytometry. It was observed that LINRIS was overexpressed in GC and showed a negative correlation with mature miR-34a, but not miR-34a precursor. In GC cells, LINRIS siRNA silencing upregulated mature miR-34a level, but not miR-34a precursor level. LINRIS overexpression downregulated miR-34a level. Cell apoptosis analysis showed that LINRIS siRNA silencing and miR-34a overexpression promoted GC cell apoptosis and suppressed cell migration and invasion, while LINRIS overexpression suppressed cell apoptosis and enhanced cell migration and invasion. In addition, the effect of LINRIS overexpression was reversed by miR-34a overexpression. Therefore, LINRIS siRNA silencing in GC may promote cell apoptosis by promoting miR-34a maturation.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"19 1","pages":"20240992"},"PeriodicalIF":1.7000,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11459274/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Open Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1515/med-2024-0992","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0

Abstract

The oncogenic role of long intergenic noncoding RNA for IGF2BP2 stability (LINRIS) has been reported in colorectal cancer. This research aimed to study its potential involvement in gastric cancer (GC). In this study, paired GC and non-tumor tissues were obtained from 64 GC patients, and the levels of LINRIS, mature microRNA-34a (miR-34a), and miR-34a precursor in these tissues were measured with RT-qPCR. Linear regression was used to analyze their correlations. The role of LINRIS overexpression and siRNA silencing in regulating the maturation of miR-34a was analyzed by RT-qPCR. Cell apoptosis was studied with flow cytometry. It was observed that LINRIS was overexpressed in GC and showed a negative correlation with mature miR-34a, but not miR-34a precursor. In GC cells, LINRIS siRNA silencing upregulated mature miR-34a level, but not miR-34a precursor level. LINRIS overexpression downregulated miR-34a level. Cell apoptosis analysis showed that LINRIS siRNA silencing and miR-34a overexpression promoted GC cell apoptosis and suppressed cell migration and invasion, while LINRIS overexpression suppressed cell apoptosis and enhanced cell migration and invasion. In addition, the effect of LINRIS overexpression was reversed by miR-34a overexpression. Therefore, LINRIS siRNA silencing in GC may promote cell apoptosis by promoting miR-34a maturation.

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
稳定 IGF2BP2 的长基因间非编码 RNA 通过抑制 microRNA-34a 的成熟抑制胃癌细胞凋亡
据报道,IGF2BP2稳定性长基因间非编码RNA(LINRIS)在结直肠癌中具有致癌作用。本研究旨在探讨其在胃癌(GC)中的潜在参与作用。本研究从 64 名胃癌患者中获取了配对的胃癌和非肿瘤组织,并通过 RT-qPCR 检测了这些组织中 LINRIS、成熟 microRNA-34a (miR-34a) 和 miR-34a 前体的水平。线性回归分析了它们之间的相关性。通过 RT-qPCR 分析了 LINRIS 过表达和 siRNA 沉默在调控 miR-34a 成熟中的作用。流式细胞术研究了细胞凋亡。结果发现,LINRIS 在 GC 中过表达,并与成熟的 miR-34a 呈负相关,但与 miR-34a 前体无关。在 GC 细胞中,LINRIS siRNA 沉默能上调成熟 miR-34a 的水平,但不能上调 miR-34a 前体的水平。过表达 LINRIS 会降低 miR-34a 的水平。细胞凋亡分析表明,LINRIS siRNA沉默和miR-34a过表达促进GC细胞凋亡,抑制细胞迁移和侵袭,而LINRIS过表达抑制细胞凋亡,增强细胞迁移和侵袭。此外,miR-34a 的过表达会逆转 LINRIS 过表达的影响。因此,在 GC 中沉默 LINRIS siRNA 可通过促进 miR-34a 成熟来促进细胞凋亡。
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
Open Medicine
Open Medicine Medicine-General Medicine
CiteScore
3.00
自引率
0.00%
发文量
153
审稿时长
20 weeks
期刊介绍: Open Medicine is an open access journal that provides users with free, instant, and continued access to all content worldwide. The primary goal of the journal has always been a focus on maintaining the high quality of its published content. Its mission is to facilitate the exchange of ideas between medical science researchers from different countries. Papers connected to all fields of medicine and public health are welcomed. Open Medicine accepts submissions of research articles, reviews, case reports, letters to editor and book reviews.
期刊最新文献
Detection of serum FOXM1 and IGF2 in patients with ARDS and their correlation with disease and prognosis. Fluoxetine inhibited RANKL-induced osteoclastic differentiation in vitro. The potential risk factors of postoperative cognitive dysfunction for endovascular therapy in acute ischemic stroke with general anesthesia. Carboplatin combined with arsenic trioxide versus carboplatin combined with docetaxel treatment for LACC: A randomized, open-label, phase II clinical study. Iron in ventricular remodeling and aneurysms post-myocardial infarction.
×
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