LncRNA AGAP11 suppresses lung adenocarcinoma progression by miR-494-3p and predicts prognosis

Ye He, Ya Lin, Chunge Dong, Jie Zhang, Yangli Zhu
{"title":"LncRNA AGAP11 suppresses lung adenocarcinoma progression by miR-494-3p and predicts prognosis","authors":"Ye He, Ya Lin, Chunge Dong, Jie Zhang, Yangli Zhu","doi":"10.1615/jenvironpatholtoxicoloncol.2024052122","DOIUrl":null,"url":null,"abstract":"Lung adenocarcinoma (LUAD) is a subtype of lung cancer that occurs frequently and results in high mortality and morbidity, comprising almost 50% of all cases with the disease. Previously, long non-coding RNAs (lncRNAs) was evidenced to be helpful in the diagnosis and prognosis of LUAD. lncRNA AGAP11 was identified as a dysregulated lncRNA in LUAD. Whether AGAP11 is linked to the progression and prognosis of LUAD has not been known. The purpose was to probe the action of AGAP11 in the LUAD progression together with its intrinsic mechanism, with a view to supplying a perspective biomarker and therapeutic target for LUAD. AGAP11 expression in LUAD was analyzed by searching in the GEPIA database and conducting RT-qPCR. The significance of AGAP11 for the prognosis of LUAD was assessed by statistical analyses. The targeting relationship between AGAP11 and miR-494-3p was corroborated with Dual-luciferase reporter assay. The role of AGAP11 on cellular processes in LUAD cells was evaluated by CCK-8 and Transwell assays. AGAP11 was markedly down-regulated in LUAD and tightly correlated with TNM stage, lymph node metastasis, and tumor differentiation degree of patients. Down-regulation of AGAP11 was found to predict a dismal prognosis of LUAD. AGAP11 negatively modulated miR-494-3p expression by interacting with it. The growth, migration, and invasion of LUAD cells could be impaired by AGAP11 overexpression, which would be attenuated by the enhanced miR-494-3p expression. AGAP11 acted as a predictor for prognosis and curbed LUAD progression through modulating miR-494-3p.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"10 1","pages":""},"PeriodicalIF":2.1000,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Environmental Pathology Toxicology and Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024052122","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"TOXICOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Lung adenocarcinoma (LUAD) is a subtype of lung cancer that occurs frequently and results in high mortality and morbidity, comprising almost 50% of all cases with the disease. Previously, long non-coding RNAs (lncRNAs) was evidenced to be helpful in the diagnosis and prognosis of LUAD. lncRNA AGAP11 was identified as a dysregulated lncRNA in LUAD. Whether AGAP11 is linked to the progression and prognosis of LUAD has not been known. The purpose was to probe the action of AGAP11 in the LUAD progression together with its intrinsic mechanism, with a view to supplying a perspective biomarker and therapeutic target for LUAD. AGAP11 expression in LUAD was analyzed by searching in the GEPIA database and conducting RT-qPCR. The significance of AGAP11 for the prognosis of LUAD was assessed by statistical analyses. The targeting relationship between AGAP11 and miR-494-3p was corroborated with Dual-luciferase reporter assay. The role of AGAP11 on cellular processes in LUAD cells was evaluated by CCK-8 and Transwell assays. AGAP11 was markedly down-regulated in LUAD and tightly correlated with TNM stage, lymph node metastasis, and tumor differentiation degree of patients. Down-regulation of AGAP11 was found to predict a dismal prognosis of LUAD. AGAP11 negatively modulated miR-494-3p expression by interacting with it. The growth, migration, and invasion of LUAD cells could be impaired by AGAP11 overexpression, which would be attenuated by the enhanced miR-494-3p expression. AGAP11 acted as a predictor for prognosis and curbed LUAD progression through modulating miR-494-3p.
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
LncRNA AGAP11通过miR-494-3p抑制肺腺癌进展并预测预后
肺腺癌(LUAD)是肺癌的一种常见亚型,死亡率和发病率都很高,几乎占所有肺癌病例的50%。此前,长非编码 RNA(lncRNA)被证明有助于 LUAD 的诊断和预后。AGAP11是否与LUAD的进展和预后有关尚未可知。本研究的目的是探究 AGAP11 在 LUAD 病程进展中的作用及其内在机制,以期为 LUAD 的生物标志物和治疗靶点提供一个视角。通过检索 GEPIA 数据库和 RT-qPCR 分析了 AGAP11 在 LUAD 中的表达。通过统计分析评估了AGAP11对LUAD预后的意义。双荧光素酶报告实验证实了 AGAP11 与 miR-494-3p 之间的靶向关系。CCK-8和Transwell试验评估了AGAP11对LUAD细胞过程的作用。AGAP11在LUAD中明显下调,并与患者的TNM分期、淋巴结转移和肿瘤分化程度密切相关。研究发现,AGAP11的下调预示着LUAD的不良预后。AGAP11通过与miR-494-3p相互作用负向调节miR-494-3p的表达。AGAP11的过表达会影响LUAD细胞的生长、迁移和侵袭,而miR-494-3p的表达增强则会减弱这种影响。AGAP11可预测预后,并通过调节miR-494-3p抑制LUAD的进展。
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
3.80
自引率
0.00%
发文量
20
审稿时长
>12 weeks
期刊介绍: The Journal of Environmental Pathology, Toxicology and Oncology publishes original research and reviews of factors and conditions that affect human and animal carcinogensis. Scientists in various fields of biological research, such as toxicologists, chemists, immunologists, pharmacologists, oncologists, pneumologists, and industrial technologists, will find this journal useful in their research on the interface between the environment, humans, and animals.
期刊最新文献
Ethyl Acetate Extract of Oratosquilla Inhibits the Growth of Nasopharyngeal Carcinoma through the Hippo Pathway Molecular mechanism of lncRNAs in ovarian cancer: lncRNA CASC19 regulates the malignant progression of ovarian cancer through miR-761/CBX2 axis LncRNA linc01105 inhibits gastric cancer growth and metastasis by regulating the miR-650/TCEA3 axis Identification of Lung Adenocarcinoma Subtypes by Using Growth Hormone-Releasing Hormone-Related Genes and Establishment of Signature to Predict Prognosis and Guide Immunother Analysis of the clinical value of hsa_circ_0001955 in papillary thyroid cancer treated with 131 iodine
×
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