LncRNA XIST的沉默通过调节miR-204/FN1轴抑制甲状腺乳头状癌的肿瘤生长和转移

IF 4.3 3区 化学 Q2 CHEMISTRY, MULTIDISCIPLINARY
Jie Qiu, Maolin Sun, Zuorong Qin, Mingbo Liu and Wenwei Zhang*, 
{"title":"LncRNA XIST的沉默通过调节miR-204/FN1轴抑制甲状腺乳头状癌的肿瘤生长和转移","authors":"Jie Qiu,&nbsp;Maolin Sun,&nbsp;Zuorong Qin,&nbsp;Mingbo Liu and Wenwei Zhang*,&nbsp;","doi":"10.1021/acsomega.5c0039010.1021/acsomega.5c00390","DOIUrl":null,"url":null,"abstract":"<p >Papillary thyroid carcinoma (PTC) is a prevalent endocrine malignancy with a high incidence rate of regional lymph node metastasis. Dysregulation of lncRNA XIST has been observed in various malignancies. This study aims to elucidate the molecular mechanism of lncRNA XIST in PTC metastasis. Quantitative real-time PCR assays were conducted to detect the expression levels of XIST, FN1, and miR-204–5p in PTC tissues. Meanwhile, loss-of-function assays were employed to evaluate the oncogenic roles of XIST in PTC cell lines. Our results revealed significant overexpression of XIST and FN1 in PTC tissues and cell lines, accompanied by decreased levels of miR-204–5p (<i>p</i> &lt; 0.05). Knockdown of XIST or FN1 inhibited cellular proliferation, metastasis, and invasion in PTC cells, upregulated E-cadherin, and downregulated N-cadherin and Vimentin. Furthermore, we demonstrated that XIST regulates FN1 expression by competitively binding to miR-204–5p. MiRNA inhibitor rescue assays confirmed the pivotal role of the XIST/miR-204/FN1 axis in PTC metastasis and invasion. Our study underscores the oncogenic role of XIST in PTC by acting as a sponge for miR-204, regulating FN1 expression. These findings hold promise for advancing our understanding of thyroid cancer and developing potential therapeutic and diagnostic targets for PTC.</p>","PeriodicalId":22,"journal":{"name":"ACS Omega","volume":"10 19","pages":"19643–19654 19643–19654"},"PeriodicalIF":4.3000,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://pubs.acs.org/doi/epdf/10.1021/acsomega.5c00390","citationCount":"0","resultStr":"{\"title\":\"Silencing of LncRNA XIST Suppressed Tumor Growth and Metastasis in Papillary Thyroid Carcinoma by Modulating miR-204/FN1 Axis\",\"authors\":\"Jie Qiu,&nbsp;Maolin Sun,&nbsp;Zuorong Qin,&nbsp;Mingbo Liu and Wenwei Zhang*,&nbsp;\",\"doi\":\"10.1021/acsomega.5c0039010.1021/acsomega.5c00390\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p >Papillary thyroid carcinoma (PTC) is a prevalent endocrine malignancy with a high incidence rate of regional lymph node metastasis. Dysregulation of lncRNA XIST has been observed in various malignancies. This study aims to elucidate the molecular mechanism of lncRNA XIST in PTC metastasis. Quantitative real-time PCR assays were conducted to detect the expression levels of XIST, FN1, and miR-204–5p in PTC tissues. Meanwhile, loss-of-function assays were employed to evaluate the oncogenic roles of XIST in PTC cell lines. Our results revealed significant overexpression of XIST and FN1 in PTC tissues and cell lines, accompanied by decreased levels of miR-204–5p (<i>p</i> &lt; 0.05). Knockdown of XIST or FN1 inhibited cellular proliferation, metastasis, and invasion in PTC cells, upregulated E-cadherin, and downregulated N-cadherin and Vimentin. Furthermore, we demonstrated that XIST regulates FN1 expression by competitively binding to miR-204–5p. MiRNA inhibitor rescue assays confirmed the pivotal role of the XIST/miR-204/FN1 axis in PTC metastasis and invasion. Our study underscores the oncogenic role of XIST in PTC by acting as a sponge for miR-204, regulating FN1 expression. These findings hold promise for advancing our understanding of thyroid cancer and developing potential therapeutic and diagnostic targets for PTC.</p>\",\"PeriodicalId\":22,\"journal\":{\"name\":\"ACS Omega\",\"volume\":\"10 19\",\"pages\":\"19643–19654 19643–19654\"},\"PeriodicalIF\":4.3000,\"publicationDate\":\"2025-05-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://pubs.acs.org/doi/epdf/10.1021/acsomega.5c00390\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ACS Omega\",\"FirstCategoryId\":\"92\",\"ListUrlMain\":\"https://pubs.acs.org/doi/10.1021/acsomega.5c00390\",\"RegionNum\":3,\"RegionCategory\":\"化学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CHEMISTRY, MULTIDISCIPLINARY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Omega","FirstCategoryId":"92","ListUrlMain":"https://pubs.acs.org/doi/10.1021/acsomega.5c00390","RegionNum":3,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CHEMISTRY, MULTIDISCIPLINARY","Score":null,"Total":0}
引用次数: 0

摘要

甲状腺乳头状癌(PTC)是一种常见的内分泌恶性肿瘤,多发于局部淋巴结转移。lncRNA XIST的失调已在多种恶性肿瘤中被观察到。本研究旨在阐明lncRNA XIST在PTC转移中的分子机制。采用实时荧光定量PCR检测PTC组织中XIST、FN1、miR-204-5p的表达水平。同时,采用功能缺失法评估XIST在PTC细胞系中的致癌作用。我们的研究结果显示,XIST和FN1在PTC组织和细胞系中显著过表达,同时miR-204-5p水平降低(p <;0.05)。敲低XIST或FN1抑制PTC细胞的增殖、转移和侵袭,上调E-cadherin,下调N-cadherin和Vimentin。此外,我们证明XIST通过竞争性结合miR-204-5p调节FN1的表达。MiRNA抑制剂挽救实验证实了XIST/miR-204/FN1轴在PTC转移和侵袭中的关键作用。我们的研究强调了XIST在PTC中的致癌作用,通过充当miR-204的海绵,调节FN1的表达。这些发现有望提高我们对甲状腺癌的认识,并开发潜在的PTC治疗和诊断靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Silencing of LncRNA XIST Suppressed Tumor Growth and Metastasis in Papillary Thyroid Carcinoma by Modulating miR-204/FN1 Axis

Papillary thyroid carcinoma (PTC) is a prevalent endocrine malignancy with a high incidence rate of regional lymph node metastasis. Dysregulation of lncRNA XIST has been observed in various malignancies. This study aims to elucidate the molecular mechanism of lncRNA XIST in PTC metastasis. Quantitative real-time PCR assays were conducted to detect the expression levels of XIST, FN1, and miR-204–5p in PTC tissues. Meanwhile, loss-of-function assays were employed to evaluate the oncogenic roles of XIST in PTC cell lines. Our results revealed significant overexpression of XIST and FN1 in PTC tissues and cell lines, accompanied by decreased levels of miR-204–5p (p < 0.05). Knockdown of XIST or FN1 inhibited cellular proliferation, metastasis, and invasion in PTC cells, upregulated E-cadherin, and downregulated N-cadherin and Vimentin. Furthermore, we demonstrated that XIST regulates FN1 expression by competitively binding to miR-204–5p. MiRNA inhibitor rescue assays confirmed the pivotal role of the XIST/miR-204/FN1 axis in PTC metastasis and invasion. Our study underscores the oncogenic role of XIST in PTC by acting as a sponge for miR-204, regulating FN1 expression. These findings hold promise for advancing our understanding of thyroid cancer and developing potential therapeutic and diagnostic targets for PTC.

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
ACS Omega
ACS Omega Chemical Engineering-General Chemical Engineering
CiteScore
6.60
自引率
4.90%
发文量
3945
审稿时长
2.4 months
期刊介绍: ACS Omega is an open-access global publication for scientific articles that describe new findings in chemistry and interfacing areas of science, without any perceived evaluation of immediate impact.
×
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:604180095
Book学术官方微信