Pan-cancer analysis and experimental validation reveal UTP4 as a novel biomarker for gastric cancer.

IF 1.9 Q4 ONCOLOGY
Molecular and clinical oncology Pub Date : 2026-02-13 eCollection Date: 2026-04-01 DOI:10.3892/mco.2026.2933
Diao Wei, Tianyu Lei, Yuhang Che, Qinyong Hu
{"title":"Pan-cancer analysis and experimental validation reveal UTP4 as a novel biomarker for gastric cancer.","authors":"Diao Wei, Tianyu Lei, Yuhang Che, Qinyong Hu","doi":"10.3892/mco.2026.2933","DOIUrl":null,"url":null,"abstract":"<p><p>UTP4 is a critical component of ribosome biogenesis, and its dysregulation may contribute to cancer development. However, the role of UTP4 in cancer remains unclear. The present study comprehensively investigated the expression and prognostic significance of UTP4 across multiple cancers, with a particular focus on gastric cancer (GC). Integrated bioinformatics analysis of public datasets, including The Cancer Genome Atlas, revealed that UTP4 is frequently overexpressed in various tumors and associated with poor prognosis. Further analysis uncovered its correlations with genetic mutations, immune infiltration and immune checkpoint expression. Based on these findings and CRISPR-Cas9 screening predictions, the functional role of UTP4 in GC cells was experimentally validated. The results demonstrated that UTP4 knockdown significantly inhibited cell proliferation, migration and invasion. These findings highlight UTP4 as a novel pan-cancer biomarker and potential therapeutic target, providing a foundation for further clinical investigations.</p>","PeriodicalId":18737,"journal":{"name":"Molecular and clinical oncology","volume":"24 4","pages":"24"},"PeriodicalIF":1.9000,"publicationDate":"2026-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12977186/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular and clinical oncology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3892/mco.2026.2933","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/4/1 0:00:00","PubModel":"eCollection","JCR":"Q4","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

UTP4 is a critical component of ribosome biogenesis, and its dysregulation may contribute to cancer development. However, the role of UTP4 in cancer remains unclear. The present study comprehensively investigated the expression and prognostic significance of UTP4 across multiple cancers, with a particular focus on gastric cancer (GC). Integrated bioinformatics analysis of public datasets, including The Cancer Genome Atlas, revealed that UTP4 is frequently overexpressed in various tumors and associated with poor prognosis. Further analysis uncovered its correlations with genetic mutations, immune infiltration and immune checkpoint expression. Based on these findings and CRISPR-Cas9 screening predictions, the functional role of UTP4 in GC cells was experimentally validated. The results demonstrated that UTP4 knockdown significantly inhibited cell proliferation, migration and invasion. These findings highlight UTP4 as a novel pan-cancer biomarker and potential therapeutic target, providing a foundation for further clinical investigations.

泛癌分析和实验验证表明,UTP4是一种新的胃癌生物标志物。
UTP4是核糖体生物发生的关键组成部分,其失调可能有助于癌症的发展。然而,UTP4在癌症中的作用尚不清楚。本研究全面研究了UTP4在多种癌症中的表达及其预后意义,特别关注胃癌(GC)。对包括The Cancer Genome Atlas在内的公共数据集的综合生物信息学分析显示,UTP4在各种肿瘤中经常过表达,并与不良预后相关。进一步分析发现其与基因突变、免疫浸润和免疫检查点表达相关。基于这些发现和CRISPR-Cas9筛选预测,实验验证了UTP4在GC细胞中的功能作用。结果表明,UTP4敲低显著抑制细胞增殖、迁移和侵袭。这些发现突出了UTP4作为一种新的泛癌症生物标志物和潜在的治疗靶点,为进一步的临床研究提供了基础。
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
CiteScore
2.80
自引率
0.00%
发文量
108
×
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