下调整合素β1抑制膀胱癌细胞增殖并促进细胞凋亡。

IF 5 3区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
BioFactors Pub Date : 2024-12-07 DOI:10.1002/biof.2150
Jin-feng Wang, Jian-she Wang, Yang Liu, Bo Ji, Bei-chen Ding, Ya-xuan Wang, Ming-hua Ren
{"title":"下调整合素β1抑制膀胱癌细胞增殖并促进细胞凋亡。","authors":"Jin-feng Wang,&nbsp;Jian-she Wang,&nbsp;Yang Liu,&nbsp;Bo Ji,&nbsp;Bei-chen Ding,&nbsp;Ya-xuan Wang,&nbsp;Ming-hua Ren","doi":"10.1002/biof.2150","DOIUrl":null,"url":null,"abstract":"<p>Bladder cancer (BC) is the most common urinary tract malignancy. Identifying biomarkers that predict prognosis and immune function in patients with BC can enhance our understanding of its pathogenesis and provide valuable guidance for diagnosis and treatment. Our findings indicate that increased ITGB1 expression is associated with higher clinical grade and stage, establishing ITGB1 as an independent prognostic risk factor for BC. Enrichment analysis revealed that the function of ITGB1 in BC was linked to the extracellular matrix. The experimental results showed that ITGB1 knockdown in the BC cell lines 5637 and RT112 reduced their proliferation, migration, and invasion. Furthermore, ITGB1 suppression promotes apoptosis in BC cells by inhibiting the PI3K-AKT pathway. A prognostic risk model incorporating CES1, NTNG1, SETBP1, and AIFM3 was developed based on ITGB1, this model can accurately predict patient prognosis based on immunological status. In conclusion, this study shows that knockdown of ITGB1 can restrain the migratory and invasive capabilities of BC cells and accelerate apoptosis, and this role might be associated with PI3K-AKT, highlighting its potential as a diagnostic marker and therapeutic target for BC.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"51 1","pages":""},"PeriodicalIF":5.0000,"publicationDate":"2024-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Knockdown of integrin β1 inhibits proliferation and promotes apoptosis in bladder cancer cells\",\"authors\":\"Jin-feng Wang,&nbsp;Jian-she Wang,&nbsp;Yang Liu,&nbsp;Bo Ji,&nbsp;Bei-chen Ding,&nbsp;Ya-xuan Wang,&nbsp;Ming-hua Ren\",\"doi\":\"10.1002/biof.2150\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Bladder cancer (BC) is the most common urinary tract malignancy. Identifying biomarkers that predict prognosis and immune function in patients with BC can enhance our understanding of its pathogenesis and provide valuable guidance for diagnosis and treatment. Our findings indicate that increased ITGB1 expression is associated with higher clinical grade and stage, establishing ITGB1 as an independent prognostic risk factor for BC. Enrichment analysis revealed that the function of ITGB1 in BC was linked to the extracellular matrix. The experimental results showed that ITGB1 knockdown in the BC cell lines 5637 and RT112 reduced their proliferation, migration, and invasion. Furthermore, ITGB1 suppression promotes apoptosis in BC cells by inhibiting the PI3K-AKT pathway. A prognostic risk model incorporating CES1, NTNG1, SETBP1, and AIFM3 was developed based on ITGB1, this model can accurately predict patient prognosis based on immunological status. In conclusion, this study shows that knockdown of ITGB1 can restrain the migratory and invasive capabilities of BC cells and accelerate apoptosis, and this role might be associated with PI3K-AKT, highlighting its potential as a diagnostic marker and therapeutic target for BC.</p>\",\"PeriodicalId\":8923,\"journal\":{\"name\":\"BioFactors\",\"volume\":\"51 1\",\"pages\":\"\"},\"PeriodicalIF\":5.0000,\"publicationDate\":\"2024-12-07\",\"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.2150\",\"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}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"BioFactors","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/biof.2150","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

摘要

膀胱癌(BC)是最常见的泌尿道恶性肿瘤。发现预测BC患者预后和免疫功能的生物标志物,可以提高我们对其发病机制的认识,并为诊断和治疗提供有价值的指导。我们的研究结果表明,ITGB1表达增加与更高的临床分级和分期相关,确立了ITGB1作为BC的独立预后危险因素。富集分析显示ITGB1在BC中的功能与细胞外基质有关。实验结果表明,ITGB1敲低在BC细胞系5637和RT112中可降低其增殖、迁移和侵袭能力。此外,ITGB1抑制通过抑制PI3K-AKT通路促进BC细胞凋亡。以ITGB1为基础,建立了包含CES1、NTNG1、SETBP1、AIFM3的预后风险模型,该模型能够基于免疫状态准确预测患者预后。综上所述,本研究表明,ITGB1的下调可以抑制BC细胞的迁移和侵袭能力,加速细胞凋亡,这种作用可能与PI3K-AKT有关,突出了其作为BC诊断标志物和治疗靶点的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Knockdown of integrin β1 inhibits proliferation and promotes apoptosis in bladder cancer cells

Bladder cancer (BC) is the most common urinary tract malignancy. Identifying biomarkers that predict prognosis and immune function in patients with BC can enhance our understanding of its pathogenesis and provide valuable guidance for diagnosis and treatment. Our findings indicate that increased ITGB1 expression is associated with higher clinical grade and stage, establishing ITGB1 as an independent prognostic risk factor for BC. Enrichment analysis revealed that the function of ITGB1 in BC was linked to the extracellular matrix. The experimental results showed that ITGB1 knockdown in the BC cell lines 5637 and RT112 reduced their proliferation, migration, and invasion. Furthermore, ITGB1 suppression promotes apoptosis in BC cells by inhibiting the PI3K-AKT pathway. A prognostic risk model incorporating CES1, NTNG1, SETBP1, and AIFM3 was developed based on ITGB1, this model can accurately predict patient prognosis based on immunological status. In conclusion, this study shows that knockdown of ITGB1 can restrain the migratory and invasive capabilities of BC cells and accelerate apoptosis, and this role might be associated with PI3K-AKT, highlighting its potential as a diagnostic marker and therapeutic target for BC.

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
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:481959085
Book学术官方微信