LINC00858 通过靶向 miR-653-5p 促进了 Wilms 肿瘤的恶性发展。

IF 4.7 4区 医学 N/A MEDICINE, GENERAL & INTERNAL
Minerva medica Pub Date : 2024-06-01 Epub Date: 2020-06-12 DOI:10.23736/S0026-4806.20.06566-0
Dan Zhou, Jilan Wang, Suping Xu, Zengming Li, Dan Kou
{"title":"LINC00858 通过靶向 miR-653-5p 促进了 Wilms 肿瘤的恶性发展。","authors":"Dan Zhou, Jilan Wang, Suping Xu, Zengming Li, Dan Kou","doi":"10.23736/S0026-4806.20.06566-0","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>To uncover the clinical significance of LINC00858 in the development of Wilms' Tumor and the potential molecular mechanism.</p><p><strong>Methods: </strong>LINC00858 levels in Wilms' Tumor species and cell lines were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The clinical significance of LINC00858 in influencing pathological features and prognosis in patients with Wilms' Tumor was analyzed. Proliferative and migratory changes in Wilms' Tumor cells with LINC00858 knockdown were assessed. The downstream gene of LINC00858 was verified by luciferase assay, and its involvement in the development of Wilms' Tumor was further explored.</p><p><strong>Results: </strong>LINC00858 was highly expressed in Wilms' Tumor tissues and cell lines. High level of LINC00858 was correlated to high rate of lymphatic metastasis and poor prognosis in patients with Wilms' Tumor. Knockdown of LINC00858 suppressed proliferative and migratory potentials in HFWT and 17-94 cells. MiR-653-5p was targeted by LINC00858. It was lowly expressed in Wilms' Tumor tissues and negatively regulated by LINC00858. Knockdown of miR-653-5p partially abolished the regulatory effects of LINC00858 on proliferative and migratory potentials in Wilms' Tumor cells.</p><p><strong>Conclusions: </strong>LINC00858 is highly expressed in Wilms' Tumor species and correlated to lymphatic metastasis rate and overall survival in patients with Wilms' Tumor. Knockdown of LINC00858 suppresses Wilms' Tumor cells to proliferate and migrate via targeting miR-653-3p.</p>","PeriodicalId":18671,"journal":{"name":"Minerva medica","volume":null,"pages":null},"PeriodicalIF":4.7000,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"LINC00858 facilitates the malignant development of Wilms' Tumor by targeting miR-653-5p.\",\"authors\":\"Dan Zhou, Jilan Wang, Suping Xu, Zengming Li, Dan Kou\",\"doi\":\"10.23736/S0026-4806.20.06566-0\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>To uncover the clinical significance of LINC00858 in the development of Wilms' Tumor and the potential molecular mechanism.</p><p><strong>Methods: </strong>LINC00858 levels in Wilms' Tumor species and cell lines were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The clinical significance of LINC00858 in influencing pathological features and prognosis in patients with Wilms' Tumor was analyzed. Proliferative and migratory changes in Wilms' Tumor cells with LINC00858 knockdown were assessed. The downstream gene of LINC00858 was verified by luciferase assay, and its involvement in the development of Wilms' Tumor was further explored.</p><p><strong>Results: </strong>LINC00858 was highly expressed in Wilms' Tumor tissues and cell lines. High level of LINC00858 was correlated to high rate of lymphatic metastasis and poor prognosis in patients with Wilms' Tumor. Knockdown of LINC00858 suppressed proliferative and migratory potentials in HFWT and 17-94 cells. MiR-653-5p was targeted by LINC00858. It was lowly expressed in Wilms' Tumor tissues and negatively regulated by LINC00858. Knockdown of miR-653-5p partially abolished the regulatory effects of LINC00858 on proliferative and migratory potentials in Wilms' Tumor cells.</p><p><strong>Conclusions: </strong>LINC00858 is highly expressed in Wilms' Tumor species and correlated to lymphatic metastasis rate and overall survival in patients with Wilms' Tumor. Knockdown of LINC00858 suppresses Wilms' Tumor cells to proliferate and migrate via targeting miR-653-3p.</p>\",\"PeriodicalId\":18671,\"journal\":{\"name\":\"Minerva medica\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":4.7000,\"publicationDate\":\"2024-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Minerva medica\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.23736/S0026-4806.20.06566-0\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2020/6/12 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"N/A\",\"JCRName\":\"MEDICINE, GENERAL & INTERNAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Minerva medica","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.23736/S0026-4806.20.06566-0","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/6/12 0:00:00","PubModel":"Epub","JCR":"N/A","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0

摘要

背景:揭示LINC00858在Wilms's肿瘤发生中的临床意义及潜在的分子机制:揭示LINC00858在Wilms's肿瘤发生发展中的临床意义和潜在的分子机制:方法:通过实时定量聚合酶链式反应(qRT-PCR)测定Wilms'肿瘤物种和细胞系中的LINC00858水平。分析了 LINC00858 在影响 Wilms 肿瘤患者病理特征和预后方面的临床意义。评估了 LINC00858 基因敲除后 Wilms 肿瘤细胞的增殖和迁移变化。通过荧光素酶实验验证了LINC00858的下游基因,并进一步探讨了其在Wilms'肿瘤发生发展中的参与作用:结果:LINC00858在Wilms'肿瘤组织和细胞系中高表达。结果:LINC00858在Wilms'肿瘤组织和细胞系中高表达,其高水平与Wilms'肿瘤患者的高淋巴转移率和预后不良相关。敲除 LINC00858 可抑制 HFWT 和 17-94 细胞的增殖和迁移潜能。LINC00858靶向了MiR-653-5p。它在 Wilms 肿瘤组织中低表达,并受 LINC00858 的负调控。敲除 miR-653-5p 可部分消除 LINC00858 对 Wilms 肿瘤细胞增殖和迁移潜能的调控作用:LINC00858在Wilms'肿瘤中高表达,并与Wilms'肿瘤患者的淋巴转移率和总生存率相关。敲除 LINC00858 可通过靶向 miR-653-3p 抑制 Wilms 肿瘤细胞的增殖和迁移。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LINC00858 facilitates the malignant development of Wilms' Tumor by targeting miR-653-5p.

Background: To uncover the clinical significance of LINC00858 in the development of Wilms' Tumor and the potential molecular mechanism.

Methods: LINC00858 levels in Wilms' Tumor species and cell lines were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The clinical significance of LINC00858 in influencing pathological features and prognosis in patients with Wilms' Tumor was analyzed. Proliferative and migratory changes in Wilms' Tumor cells with LINC00858 knockdown were assessed. The downstream gene of LINC00858 was verified by luciferase assay, and its involvement in the development of Wilms' Tumor was further explored.

Results: LINC00858 was highly expressed in Wilms' Tumor tissues and cell lines. High level of LINC00858 was correlated to high rate of lymphatic metastasis and poor prognosis in patients with Wilms' Tumor. Knockdown of LINC00858 suppressed proliferative and migratory potentials in HFWT and 17-94 cells. MiR-653-5p was targeted by LINC00858. It was lowly expressed in Wilms' Tumor tissues and negatively regulated by LINC00858. Knockdown of miR-653-5p partially abolished the regulatory effects of LINC00858 on proliferative and migratory potentials in Wilms' Tumor cells.

Conclusions: LINC00858 is highly expressed in Wilms' Tumor species and correlated to lymphatic metastasis rate and overall survival in patients with Wilms' Tumor. Knockdown of LINC00858 suppresses Wilms' Tumor cells to proliferate and migrate via targeting miR-653-3p.

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
Minerva medica
Minerva medica 医学-医学:内科
CiteScore
6.40
自引率
6.40%
发文量
358
审稿时长
>12 weeks
期刊介绍: Minerva Medica publishes scientific papers on internal medicine. Manuscripts may be submitted in the form of editorials, original articles, review articles, case reports, special articles, letters to the Editor and guidelines. The journal aims to provide its readers with papers of the highest quality and impact through a process of careful peer review and editorial work. Duties and responsibilities of all the subjects involved in the editorial process are summarized at Publication ethics.
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信