SH3BP5-AS1/IGF2BP2/VDAC2轴促进膀胱癌细胞凋亡和铁下垂

IF 1 4区 医学 Q4 ONCOLOGY
Bladder Cancer Pub Date : 2023-03-31 DOI:10.3233/blc-211629
Yong Shao, Yunhui Chan, Rong Zhao
{"title":"SH3BP5-AS1/IGF2BP2/VDAC2轴促进膀胱癌细胞凋亡和铁下垂","authors":"Yong Shao, Yunhui Chan, Rong Zhao","doi":"10.3233/blc-211629","DOIUrl":null,"url":null,"abstract":"BACKGROUND: Bladder cancer (BC) is the most common malignant tumor in the urinary system with a high incidence, imposing a burden on the healthcare system worldwide. The participation of long non-coding RNAs (lncRNAs) in BC has attracted increasing attention. OBJECTIVE: The aim in the current study was to explore the potential mechanism involving SH3BP5-AS1 in modulating BC cell proliferation, apoptosis and ferroptosis. METHODS: qPCR and WB analysis measured the expression of RNAs and proteins. Functional and mechanism experiments were performed to investigate RNA impacts on cell proliferation, apoptosis and ferroptosis, and explore the correlation between RNA and protein expression. RESULTS: SH3BP5-AS1 was down-regulated in BC cells, and SH3BP5-AS1 overexpression could inhibit BC cell proliferation but facilitate the cell apoptosis. SH3BP5-AS1 was also found to facilitate the ferroptosis of BC cells. Additionally, SH3BP5-AS1 was confirmed to recruit IGF2BP2 to regulate VDAC2 expression in the m6A-dependent manner. VDAC2 was detected to be down-regulated in BC cells and was verified to inhibit BC cell growth. Moreover, it was indicated from rescue assays that SH3BP5-AS1 could modulate VDAC2 expression to promote the ferroptosis of BC cells. CONCLUSION: SH3BP5-AS1 could affect BC cell proliferation, apoptosis and ferroptosis via IGF2BP2/VDAC2, providing a novel molecular perspective for understanding BC.","PeriodicalId":54217,"journal":{"name":"Bladder Cancer","volume":null,"pages":null},"PeriodicalIF":1.0000,"publicationDate":"2023-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"SH3BP5-AS1/IGF2BP2/VDAC2 Axis Promotes the Apoptosis and Ferroptosis of Bladder Cancer Cells\",\"authors\":\"Yong Shao, Yunhui Chan, Rong Zhao\",\"doi\":\"10.3233/blc-211629\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"BACKGROUND: Bladder cancer (BC) is the most common malignant tumor in the urinary system with a high incidence, imposing a burden on the healthcare system worldwide. The participation of long non-coding RNAs (lncRNAs) in BC has attracted increasing attention. OBJECTIVE: The aim in the current study was to explore the potential mechanism involving SH3BP5-AS1 in modulating BC cell proliferation, apoptosis and ferroptosis. METHODS: qPCR and WB analysis measured the expression of RNAs and proteins. Functional and mechanism experiments were performed to investigate RNA impacts on cell proliferation, apoptosis and ferroptosis, and explore the correlation between RNA and protein expression. RESULTS: SH3BP5-AS1 was down-regulated in BC cells, and SH3BP5-AS1 overexpression could inhibit BC cell proliferation but facilitate the cell apoptosis. SH3BP5-AS1 was also found to facilitate the ferroptosis of BC cells. Additionally, SH3BP5-AS1 was confirmed to recruit IGF2BP2 to regulate VDAC2 expression in the m6A-dependent manner. VDAC2 was detected to be down-regulated in BC cells and was verified to inhibit BC cell growth. Moreover, it was indicated from rescue assays that SH3BP5-AS1 could modulate VDAC2 expression to promote the ferroptosis of BC cells. CONCLUSION: SH3BP5-AS1 could affect BC cell proliferation, apoptosis and ferroptosis via IGF2BP2/VDAC2, providing a novel molecular perspective for understanding BC.\",\"PeriodicalId\":54217,\"journal\":{\"name\":\"Bladder Cancer\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.0000,\"publicationDate\":\"2023-03-31\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Bladder Cancer\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3233/blc-211629\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bladder Cancer","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3233/blc-211629","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

背景:膀胱癌(BC)是泌尿系统最常见的恶性肿瘤,发病率高,给全球医疗保健系统带来了负担。长链非编码rna (long non-coding rna, lncRNAs)在BC中的参与越来越受到关注。目的:本研究旨在探讨SH3BP5-AS1在调节BC细胞增殖、凋亡和铁凋亡中的潜在机制。方法:qPCR和WB分析检测rna和蛋白的表达。通过功能和机制实验研究RNA对细胞增殖、凋亡和铁凋亡的影响,并探讨RNA与蛋白表达的相关性。结果:SH3BP5-AS1在BC细胞中下调表达,SH3BP5-AS1过表达可抑制BC细胞增殖,促进细胞凋亡。SH3BP5-AS1也被发现促进BC细胞铁下垂。此外,SH3BP5-AS1被证实以m6a依赖的方式招募IGF2BP2调节VDAC2的表达。在BC细胞中检测到VDAC2下调,并证实其抑制BC细胞生长。此外,挽救实验表明SH3BP5-AS1可以调节VDAC2的表达,促进BC细胞铁凋亡。结论:SH3BP5-AS1可通过IGF2BP2/VDAC2影响BC细胞增殖、凋亡和铁死亡,为了解BC提供了新的分子视角。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
SH3BP5-AS1/IGF2BP2/VDAC2 Axis Promotes the Apoptosis and Ferroptosis of Bladder Cancer Cells
BACKGROUND: Bladder cancer (BC) is the most common malignant tumor in the urinary system with a high incidence, imposing a burden on the healthcare system worldwide. The participation of long non-coding RNAs (lncRNAs) in BC has attracted increasing attention. OBJECTIVE: The aim in the current study was to explore the potential mechanism involving SH3BP5-AS1 in modulating BC cell proliferation, apoptosis and ferroptosis. METHODS: qPCR and WB analysis measured the expression of RNAs and proteins. Functional and mechanism experiments were performed to investigate RNA impacts on cell proliferation, apoptosis and ferroptosis, and explore the correlation between RNA and protein expression. RESULTS: SH3BP5-AS1 was down-regulated in BC cells, and SH3BP5-AS1 overexpression could inhibit BC cell proliferation but facilitate the cell apoptosis. SH3BP5-AS1 was also found to facilitate the ferroptosis of BC cells. Additionally, SH3BP5-AS1 was confirmed to recruit IGF2BP2 to regulate VDAC2 expression in the m6A-dependent manner. VDAC2 was detected to be down-regulated in BC cells and was verified to inhibit BC cell growth. Moreover, it was indicated from rescue assays that SH3BP5-AS1 could modulate VDAC2 expression to promote the ferroptosis of BC cells. CONCLUSION: SH3BP5-AS1 could affect BC cell proliferation, apoptosis and ferroptosis via IGF2BP2/VDAC2, providing a novel molecular perspective for understanding 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
Bladder Cancer
Bladder Cancer Medicine-Urology
CiteScore
1.60
自引率
0.00%
发文量
35
期刊介绍: Bladder Cancer is an international multidisciplinary journal to facilitate progress in understanding the epidemiology/etiology, genetics, molecular correlates, pathogenesis, pharmacology, ethics, patient advocacy and survivorship, diagnosis and treatment of tumors of the bladder and upper urinary tract. The journal publishes research reports, reviews, short communications, and letters-to-the-editor. The journal is dedicated to providing an open forum for original research in basic science, translational research and clinical medicine that expedites our fundamental understanding and improves treatment of tumors of the bladder and upper urinary tract.
×
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