Oncogenic role of lncRNA SBF2-AS1 in bladder cancer

IF 2.4 3区生物学 Q2 GENETICS & HEREDITY Gene Pub Date : 2025-01-30 Epub Date: 2024-10-30 DOI:10.1016/j.gene.2024.149061

Edymara dos Anjos Oliveira , Tamires Cunha Almeida , Glenda Nicioli da Silva

{"title":"Oncogenic role of lncRNA SBF2-AS1 in bladder cancer","authors":"Edymara dos Anjos Oliveira , Tamires Cunha Almeida , Glenda Nicioli da Silva","doi":"10.1016/j.gene.2024.149061","DOIUrl":null,"url":null,"abstract":"<div><h3>Introduction</h3><div>Bladder cancer is a malignant neoplasm with increasing incidence rates. LncRNAs play an important role in cancer, including development, prognosis, and response to therapies. It is known that lncRNA <em>SBF2-AS1</em> was associated with cell proliferation and worse prognosis in various tumor types, but its role remains incompletely understood in bladder cancer. In this context, our objective was to evaluate the effect of lncRNA <em>SBF2-AS1</em> silencing on bladder cancer cells.</div></div><div><h3>Methods</h3><div>J82 and UM-UC-3 high-grade bladder tumor cells were treated with two siRNAs specific for <em>SBF2-AS1</em> to evaluate cytotoxicity, clonogenic survival, morphology, cell migration, and cell cycle progression.</div></div><div><h3>Results</h3><div>Expression inhibition of <em>SBF2-AS1</em> resulted in cytotoxicity, morphological changes, and decreased clone formation and cell migration. Cell cycle alterations were not observed.</div></div><div><h3>Conclusion</h3><div>Our study revealed that <em>SBF2-AS1</em> plays an oncogenic role and holds promise as a potential target for the treatment of bladder cancer.</div></div>","PeriodicalId":12499,"journal":{"name":"Gene","volume":"935 ","pages":"Article 149061"},"PeriodicalIF":2.4000,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Gene","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0378111924009429","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/30 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}

引用次数: 0

Abstract

Introduction

Bladder cancer is a malignant neoplasm with increasing incidence rates. LncRNAs play an important role in cancer, including development, prognosis, and response to therapies. It is known that lncRNA SBF2-AS1 was associated with cell proliferation and worse prognosis in various tumor types, but its role remains incompletely understood in bladder cancer. In this context, our objective was to evaluate the effect of lncRNA SBF2-AS1 silencing on bladder cancer cells.

Methods

J82 and UM-UC-3 high-grade bladder tumor cells were treated with two siRNAs specific for SBF2-AS1 to evaluate cytotoxicity, clonogenic survival, morphology, cell migration, and cell cycle progression.

Results

Expression inhibition of SBF2-AS1 resulted in cytotoxicity, morphological changes, and decreased clone formation and cell migration. Cell cycle alterations were not observed.

Conclusion

Our study revealed that SBF2-AS1 plays an oncogenic role and holds promise as a potential target for the treatment of bladder cancer.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

lncRNA SBF2-AS1 在膀胱癌中的致癌作用

导言膀胱癌是一种发病率不断上升的恶性肿瘤。LncRNA 在癌症的发生、预后和治疗反应等方面发挥着重要作用。众所周知，lncRNA SBF2-AS1与多种肿瘤类型中的细胞增殖和不良预后有关，但其在膀胱癌中的作用仍不完全清楚。在这种情况下，我们的目的是评估沉默 lncRNA SBF2-AS1 对膀胱癌细胞的影响：方法：用两种特异性 SBF2-AS1 的 siRNA 处理 J82 和 UM-UC-3 高级别的膀胱肿瘤细胞，以评估细胞毒性、克隆性存活、形态、细胞迁移和细胞周期进展：结果：抑制 SBF2-AS1 的表达会导致细胞毒性、形态变化、克隆形成和细胞迁移减少。结论：我们的研究发现，SBF2-AS1 的表达抑制导致细胞毒性、形态学变化、克隆形成和细胞迁移减少，但未观察到细胞周期改变：我们的研究表明，SBF2-AS1 具有致癌作用，有望成为治疗膀胱癌的潜在靶点。

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分钟内获得全文去求助

来源期刊

Gene 生物-遗传学

CiteScore

6.10

自引率

2.90%

发文量

718

审稿时长

42 days

期刊介绍： Gene publishes papers that focus on the regulation, expression, function and evolution of genes in all biological contexts, including all prokaryotic and eukaryotic organisms, as well as viruses.