Mechanism of YTHDF2-Mediated Epigenetic Modification in the Proliferation and Invasion of Renal Cell Carcinoma Cells

IF 5.2 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
BioFactors Pub Date : 2026-04-24 DOI:10.1002/biof.70099
Xiaomeng Zhang, Yan Zhang, Xin Yang, Ye Fan, Yingying Zhu
{"title":"Mechanism of YTHDF2-Mediated Epigenetic Modification in the Proliferation and Invasion of Renal Cell Carcinoma Cells","authors":"Xiaomeng Zhang,&nbsp;Yan Zhang,&nbsp;Xin Yang,&nbsp;Ye Fan,&nbsp;Yingying Zhu","doi":"10.1002/biof.70099","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>Renal cell carcinoma (RCC) ranks as the most prevalent form of urogenital cancer. This research aims to investigate the role of YTHDF2 in the RCC progression and identify new therapeutic targets for RCC. YTHDF2, E2F2, and CORO6 were assayed via qRT-PCR and Western blot. YTHDF2 was downregulated in RCC cells, while E2F2 and CORO6 were upregulated. After overexpressing YTHDF2 in RCC cells, cell viability, proliferation, invasion, and migration were measured. m6A levels were assessed. The binding of YTHDF2 to E2F2 was detected. The E2F2 mRNA stability was detected. The binding of E2F2 to the CORO6 promoter was analyzed. Overexpression of E2F2 or CORO6 was combined with YTHDF2 overexpression to validate the mechanism. Tumor growth and metastasis were observed. Results confirmed that YTHDF2 overexpression decreased cell proliferation, invasion, and migration. YTHDF2 bound to the m6A sites on E2F2 mRNA, promoted E2F2 degradation, and inhibited E2F2 expression. E2F2 bound to the CORO6 promoter to enhance CORO6 expression. Overexpression of E2F2 or CORO6 partially reversed the suppressive effects of YTHDF2 overexpression on RCC cell proliferation and invasion. YTHDF2 overexpression suppressed tumor growth and metastasis. In conclusion, YTHDF2 overexpression suppresses RCC progression by inhibiting E2F2 expression and reducing CORO6 expression via m6A modification.</p>\n </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 2","pages":""},"PeriodicalIF":5.2000,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"BioFactors","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/biof.70099","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Renal cell carcinoma (RCC) ranks as the most prevalent form of urogenital cancer. This research aims to investigate the role of YTHDF2 in the RCC progression and identify new therapeutic targets for RCC. YTHDF2, E2F2, and CORO6 were assayed via qRT-PCR and Western blot. YTHDF2 was downregulated in RCC cells, while E2F2 and CORO6 were upregulated. After overexpressing YTHDF2 in RCC cells, cell viability, proliferation, invasion, and migration were measured. m6A levels were assessed. The binding of YTHDF2 to E2F2 was detected. The E2F2 mRNA stability was detected. The binding of E2F2 to the CORO6 promoter was analyzed. Overexpression of E2F2 or CORO6 was combined with YTHDF2 overexpression to validate the mechanism. Tumor growth and metastasis were observed. Results confirmed that YTHDF2 overexpression decreased cell proliferation, invasion, and migration. YTHDF2 bound to the m6A sites on E2F2 mRNA, promoted E2F2 degradation, and inhibited E2F2 expression. E2F2 bound to the CORO6 promoter to enhance CORO6 expression. Overexpression of E2F2 or CORO6 partially reversed the suppressive effects of YTHDF2 overexpression on RCC cell proliferation and invasion. YTHDF2 overexpression suppressed tumor growth and metastasis. In conclusion, YTHDF2 overexpression suppresses RCC progression by inhibiting E2F2 expression and reducing CORO6 expression via m6A modification.

Abstract Image

ythdf2介导的表观遗传修饰在肾癌细胞增殖和侵袭中的作用机制
肾细胞癌(RCC)是泌尿生殖系统最常见的癌症。本研究旨在探讨YTHDF2在RCC进展中的作用,并寻找新的RCC治疗靶点。采用qRT-PCR和Western blot检测YTHDF2、E2F2和CORO6。在RCC细胞中,YTHDF2下调,而E2F2和CORO6上调。在RCC细胞中过表达YTHDF2后,测量细胞活力、增殖、侵袭和迁移。评估m6A水平。检测到YTHDF2与E2F2的结合。检测E2F2 mRNA的稳定性。分析了E2F2与CORO6启动子的结合。将E2F2或CORO6过表达与YTHDF2过表达结合验证其机制。观察肿瘤生长及转移情况。结果证实,YTHDF2过表达可降低细胞增殖、侵袭和迁移。YTHDF2结合E2F2 mRNA上的m6A位点,促进E2F2降解,抑制E2F2的表达。E2F2结合CORO6启动子,增强CORO6的表达。E2F2或CORO6过表达部分逆转了YTHDF2过表达对RCC细胞增殖和侵袭的抑制作用。YTHDF2过表达抑制肿瘤生长和转移。综上所述,YTHDF2过表达通过m6A修饰抑制E2F2表达,降低CORO6表达,从而抑制RCC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 求助全文
来源期刊
BioFactors
BioFactors 生物-内分泌学与代谢
CiteScore
11.50
自引率
3.30%
发文量
96
审稿时长
6-12 weeks
期刊介绍: BioFactors, a journal of the International Union of Biochemistry and Molecular Biology, is devoted to the rapid publication of highly significant original research articles and reviews in experimental biology in health and disease. The word “biofactors” refers to the many compounds that regulate biological functions. Biological factors comprise many molecules produced or modified by living organisms, and present in many essential systems like the blood, the nervous or immunological systems. A non-exhaustive list of biological factors includes neurotransmitters, cytokines, chemokines, hormones, coagulation factors, transcription factors, signaling molecules, receptor ligands and many more. In the group of biofactors we can accommodate several classical molecules not synthetized in the body such as vitamins, micronutrients or essential trace elements. In keeping with this unified view of biochemistry, BioFactors publishes research dealing with the identification of new substances and the elucidation of their functions at the biophysical, biochemical, cellular and human level as well as studies revealing novel functions of already known biofactors. The journal encourages the submission of studies that use biochemistry, biophysics, cell and molecular biology and/or cell signaling approaches.
×
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
小红书