HNRNPC promotes progression of non-small cell lung cancer by maintaining TFAP2A mRNA stability.

IF 5.3 2区 医学 Q1 ONCOLOGY
Minghua Liao, Chunyu Li, Rui Yang, Jun Li, Ke Wu, Jiayi Zhang, Qian Zhu, Yingchang Shi, Xianming Zhang
{"title":"HNRNPC promotes progression of non-small cell lung cancer by maintaining TFAP2A mRNA stability.","authors":"Minghua Liao, Chunyu Li, Rui Yang, Jun Li, Ke Wu, Jiayi Zhang, Qian Zhu, Yingchang Shi, Xianming Zhang","doi":"10.1186/s12935-025-03660-x","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>HNRNPC is an RNA-binding protein that is overexpressed in a variety of cancers and is well known as an m6A \"reader\", but its specific function and molecular mechanism in NSCLC have not been fully understood. This study aimed to discuss molecular mechanism of HNRNPC in NSCLC.</p><p><strong>Methods: </strong>HNRNPC expression and clinically relevant data in pan-cancer and LUAD were extracted through these websites, including UALCAN, TIMER2 and GEPIA. The target gene of HNRNPC were identified through RIP-seq, meRIP-qPCR and mRNA stability test. The differential expression of target gene in NSCLC was explored by immunohistochemistry. Lentivirus was selected to knock down HNRNPC and plasmid was selected to overexpress downstream target genes. The transfection efficiency was verified by RT-qPCR and Western Blot. In vitro colony formation assay, CCK-8, wound healing, transwell assays were performed to determine the biological functions of HNRNPC and target gene in lung adenocarcinoma cells.</p><p><strong>Results: </strong>HNRNPC can promotes the expression of TFAP2A by recognizing the m6A modification of TFAP2A mRNA and maintaining its stability, activates the TFAP2A/CTNNB1 axis, enhances EMT, and ultimately promotes the malignant process of NSCLC and promote distant metastasis of NSCLC.</p><p><strong>Conclusions: </strong>These results supported that HNRNPC regulate TFAP2A to promote the malignant progression and EMT of NSCLC. These findings connect m6A modification with EMT, providing a new perspective on the regulation of m6A modification in tumors.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"85"},"PeriodicalIF":5.3000,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889907/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Cell International","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12935-025-03660-x","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: HNRNPC is an RNA-binding protein that is overexpressed in a variety of cancers and is well known as an m6A "reader", but its specific function and molecular mechanism in NSCLC have not been fully understood. This study aimed to discuss molecular mechanism of HNRNPC in NSCLC.

Methods: HNRNPC expression and clinically relevant data in pan-cancer and LUAD were extracted through these websites, including UALCAN, TIMER2 and GEPIA. The target gene of HNRNPC were identified through RIP-seq, meRIP-qPCR and mRNA stability test. The differential expression of target gene in NSCLC was explored by immunohistochemistry. Lentivirus was selected to knock down HNRNPC and plasmid was selected to overexpress downstream target genes. The transfection efficiency was verified by RT-qPCR and Western Blot. In vitro colony formation assay, CCK-8, wound healing, transwell assays were performed to determine the biological functions of HNRNPC and target gene in lung adenocarcinoma cells.

Results: HNRNPC can promotes the expression of TFAP2A by recognizing the m6A modification of TFAP2A mRNA and maintaining its stability, activates the TFAP2A/CTNNB1 axis, enhances EMT, and ultimately promotes the malignant process of NSCLC and promote distant metastasis of NSCLC.

Conclusions: These results supported that HNRNPC regulate TFAP2A to promote the malignant progression and EMT of NSCLC. These findings connect m6A modification with EMT, providing a new perspective on the regulation of m6A modification in tumors.

求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
10.90
自引率
1.70%
发文量
360
审稿时长
1 months
期刊介绍: Cancer Cell International publishes articles on all aspects of cancer cell biology, originating largely from, but not limited to, work using cell culture techniques. The journal focuses on novel cancer studies reporting data from biological experiments performed on cells grown in vitro, in two- or three-dimensional systems, and/or in vivo (animal experiments). These types of experiments have provided crucial data in many fields, from cell proliferation and transformation, to epithelial-mesenchymal interaction, to apoptosis, and host immune response to tumors. Cancer Cell International also considers articles that focus on novel technologies or novel pathways in molecular analysis and on epidemiological studies that may affect patient care, as well as articles reporting translational cancer research studies where in vitro discoveries are bridged to the clinic. As such, the journal is interested in laboratory and animal studies reporting on novel biomarkers of tumor progression and response to therapy and on their applicability to human cancers.
×
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