MicroRNA-3651 Facilitates Glioma Progression by Targeting SCN3B and Serves as a Prognostic Indicator

IF 1.1 3区医学 Q2 CLINICAL NEUROLOGY

Acta Neurologica Scandinavica Pub Date : 2026-09-18 DOI:10.1155/ane/7350637

Jun Wang, Yijun Deng, Dekang Nie, Guan Sun, Wei Zeng

{"title":"MicroRNA-3651 Facilitates Glioma Progression by Targeting SCN3B and Serves as a Prognostic Indicator","authors":"Jun Wang, Yijun Deng, Dekang Nie, Guan Sun, Wei Zeng","doi":"10.1155/ane/7350637","DOIUrl":null,"url":null,"abstract":"<div>\n \n <section>\n \n <h3> Aim</h3>\n \n <p>This study is aimed at ascertaining the expression, clinical implications, and cellular functions of miR-3651 in glioma, as well as its potential target gene, <i>Sodium Voltage-Gated Channel Beta Subunit 3</i> (<i>SCN3B</i>).</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>The expression of serum miR-3651 was determined in glioma using qRT-PCR. The relationship between miR-3651 expression and clinicopathological factors was assessed. Additionally, its prognostic value was evaluated using Cox regression analysis. The effects of miR-3651 on cellular processes were investigated, and its direct interaction with <i>SCN3B</i> was confirmed through a dual-luciferase reporter assay.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>Patients with glioma exhibited significantly elevated serum levels of miR-3651, which were strongly correlated with higher WHO grades, decreased KPS scores, and poorer prognoses (<i>p</i> < 0.001). It was established that miR-3651 serves as an independent predictor of clinical outcomes in glioma (HR = 5.387, <i>p</i> < 0.001). Inhibition of miR-3651 expression significantly reduced the proliferation, migration, and invasion of glioma cells while promoting apoptosis. The direct targeting of <i>SCN3B</i> by miR-3651 was confirmed, revealing that <i>SCN3B</i> expression was downregulated in glioma. Rescue experiments indicated that the overexpression of <i>SCN3B</i> counteracted the antitumor effects of the miR-3651 inhibitor.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>miR-3651 is a potential prognostic marker for gliomas by targeting SCN3B to promote tumor progression. However, these findings are based on serum samples and require further validation in independent cohorts.</p>\n </section>\n </div>","PeriodicalId":6939,"journal":{"name":"Acta Neurologica Scandinavica","volume":"2026 1","pages":""},"PeriodicalIF":1.1000,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/ane/7350637","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta Neurologica Scandinavica","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1155/ane/7350637","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Aim

This study is aimed at ascertaining the expression, clinical implications, and cellular functions of miR-3651 in glioma, as well as its potential target gene, Sodium Voltage-Gated Channel Beta Subunit 3 (SCN3B).

Methods

The expression of serum miR-3651 was determined in glioma using qRT-PCR. The relationship between miR-3651 expression and clinicopathological factors was assessed. Additionally, its prognostic value was evaluated using Cox regression analysis. The effects of miR-3651 on cellular processes were investigated, and its direct interaction with SCN3B was confirmed through a dual-luciferase reporter assay.

Results

Patients with glioma exhibited significantly elevated serum levels of miR-3651, which were strongly correlated with higher WHO grades, decreased KPS scores, and poorer prognoses (p < 0.001). It was established that miR-3651 serves as an independent predictor of clinical outcomes in glioma (HR = 5.387, p < 0.001). Inhibition of miR-3651 expression significantly reduced the proliferation, migration, and invasion of glioma cells while promoting apoptosis. The direct targeting of SCN3B by miR-3651 was confirmed, revealing that SCN3B expression was downregulated in glioma. Rescue experiments indicated that the overexpression of SCN3B counteracted the antitumor effects of the miR-3651 inhibitor.

Conclusion

miR-3651 is a potential prognostic marker for gliomas by targeting SCN3B to promote tumor progression. However, these findings are based on serum samples and require further validation in independent cohorts.

查看原文本刊更多论文

MicroRNA-3651通过靶向SCN3B促进胶质瘤进展并作为预后指标

本研究旨在确定miR-3651及其潜在靶基因钠电压门控通道β亚基3 （SCN3B）在胶质瘤中的表达、临床意义和细胞功能。方法采用qRT-PCR检测血清miR-3651在胶质瘤组织中的表达。评估miR-3651表达与临床病理因素的关系。此外，采用Cox回归分析评估其预后价值。我们研究了miR-3651对细胞过程的影响，并通过双荧光素酶报告基因实验证实了其与SCN3B的直接相互作用。结果胶质瘤患者血清miR-3651水平显著升高，这与WHO分级较高、KPS评分较低和预后较差密切相关（p < 0.001）。证实miR-3651是胶质瘤临床结局的独立预测因子（HR = 5.387, p < 0.001）。抑制miR-3651的表达可显著降低胶质瘤细胞的增殖、迁移和侵袭，同时促进细胞凋亡。证实了miR-3651直接靶向SCN3B，揭示了SCN3B在胶质瘤中的表达下调。抢救实验表明，SCN3B的过表达抵消了miR-3651抑制剂的抗肿瘤作用。结论miR-3651通过靶向SCN3B促进肿瘤进展，是胶质瘤的潜在预后标志物。然而，这些发现是基于血清样本的，需要在独立队列中进一步验证。

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

Acta Neurologica Scandinavica 医学-临床神经学

CiteScore

6.70

自引率

2.90%

发文量

161

审稿时长

4-8 weeks

期刊介绍： Acta Neurologica Scandinavica aims to publish manuscripts of a high scientific quality representing original clinical, diagnostic or experimental work in neuroscience. The journal''s scope is to act as an international forum for the dissemination of information advancing the science or practice of this subject area. Papers in English will be welcomed, especially those which bring new knowledge and observations from the application of therapies or techniques in the combating of a broad spectrum of neurological disease and neurodegenerative disorders. Relevant articles on the basic neurosciences will be published where they extend present understanding of such disorders. Priority will be given to review of topical subjects. Papers requiring rapid publication because of their significance and timeliness will be included as ''Clinical commentaries'' not exceeding two printed pages, as will ''Clinical commentaries'' of sufficient general interest. Debate within the speciality is encouraged in the form of ''Letters to the editor''. All submitted manuscripts falling within the overall scope of the journal will be assessed by suitably qualified referees.