β-suppressor protein 1 (ARRB1)-△exon13 modulates the progression of glioblastoma via combination with glycolysis-related proteins

IF 2.3 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochemistry and Biophysics Reports Pub Date : 2025-05-13 DOI:10.1016/j.bbrep.2025.102048

Zi-Long Wei , Shuo Han , Dong-Hua Han , Xue-Tao Li , Yu-Lun Huang , Zhi-Min Wang

{"title":"β-suppressor protein 1 (ARRB1)-△exon13 modulates the progression of glioblastoma via combination with glycolysis-related proteins","authors":"Zi-Long Wei , Shuo Han , Dong-Hua Han , Xue-Tao Li , Yu-Lun Huang , Zhi-Min Wang","doi":"10.1016/j.bbrep.2025.102048","DOIUrl":null,"url":null,"abstract":"<div><div>Glioblastoma multiform (GBM) constitutes approximately 14.7 % of all central nervous system tumors (CNSTs) and 45.2 % of primary malignant CNSTs. Extensive research has indicated that β-arrestin 1 (ARRB1) plays a significant role in tumor malignancy. In this investigation, we established GBM cell lines representing normal control (NC), overexpression (OE) and Δexon13 GBM variants (△exon13) of ARRB1. Our findings indicate that the ARRB1-OE isoform facilitated GBM cell proliferation and migration, with the ARRB1-△exon13 isoform further augmenting this effect. Notably, the isoform ARRB1-△exon13 binds to glycolytic proteins including ENO1 and ALDOA and regulates glycolysis. In vivo studies corroborate the tumor-promoting effects of ARRB1-Δexon13. Furthermore, we demonstrate that 2-DG effectively inhibits the malignancy-promoting capabilities of ARRB1-Δexon13 by reducing pyruvate levels. Our identification of alternative RNA splicing events of ARRB1 reveals a mechanism by which GBM cell malignancy is augmented through ARRB1-Δexon13, which mediates glycolysis-related pathways.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"42 ","pages":"Article 102048"},"PeriodicalIF":2.3000,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemistry and Biophysics Reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2405580825001359","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Glioblastoma multiform (GBM) constitutes approximately 14.7 % of all central nervous system tumors (CNSTs) and 45.2 % of primary malignant CNSTs. Extensive research has indicated that β-arrestin 1 (ARRB1) plays a significant role in tumor malignancy. In this investigation, we established GBM cell lines representing normal control (NC), overexpression (OE) and Δexon13 GBM variants (△exon13) of ARRB1. Our findings indicate that the ARRB1-OE isoform facilitated GBM cell proliferation and migration, with the ARRB1-△exon13 isoform further augmenting this effect. Notably, the isoform ARRB1-△exon13 binds to glycolytic proteins including ENO1 and ALDOA and regulates glycolysis. In vivo studies corroborate the tumor-promoting effects of ARRB1-Δexon13. Furthermore, we demonstrate that 2-DG effectively inhibits the malignancy-promoting capabilities of ARRB1-Δexon13 by reducing pyruvate levels. Our identification of alternative RNA splicing events of ARRB1 reveals a mechanism by which GBM cell malignancy is augmented through ARRB1-Δexon13, which mediates glycolysis-related pathways.

Abstract Image

查看原文本刊更多论文

β-抑制蛋白1 (ARRB1)-△外显子13通过与糖酵解相关蛋白联合调节胶质母细胞瘤的进展

多形性胶质母细胞瘤（GBM）约占所有中枢神经系统肿瘤（CNSTs）的14.7%，占原发性恶性CNSTs的45.2%。大量研究表明，β-阻滞蛋白1 （ARRB1）在肿瘤恶性过程中发挥着重要作用。在这项研究中，我们建立了具有ARRB1正常对照（NC）、过表达（OE）和Δexon13 GBM变体（△exon13）的GBM细胞系。我们的研究结果表明，ARRB1- oe亚型促进了GBM细胞的增殖和迁移，而ARRB1-△外显子13亚型进一步增强了这一作用。值得注意的是，同种异构体ARRB1-△外显子13与糖酵解蛋白（包括ENO1和ALDOA）结合并调节糖酵解。体内研究证实了ARRB1的促肿瘤作用-Δexon13。此外，我们证明2-DG通过降低丙酮酸水平有效抑制ARRB1-Δexon13的恶性肿瘤促进能力。我们对ARRB1的选择性RNA剪接事件的鉴定揭示了通过ARRB1-Δexon13介导糖酵解相关途径增强GBM细胞恶性肿瘤的机制。

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

Biochemistry and Biophysics Reports Biochemistry, Genetics and Molecular Biology-Biophysics

CiteScore

4.60

自引率

0.00%

发文量

191

审稿时长

59 days

期刊介绍： Open access, online only, peer-reviewed international journal in the Life Sciences, established in 2014 Biochemistry and Biophysics Reports (BB Reports) publishes original research in all aspects of Biochemistry, Biophysics and related areas like Molecular and Cell Biology. BB Reports welcomes solid though more preliminary, descriptive and small scale results if they have the potential to stimulate and/or contribute to future research, leading to new insights or hypothesis. Primary criteria for acceptance is that the work is original, scientifically and technically sound and provides valuable knowledge to life sciences research. We strongly believe all results deserve to be published and documented for the advancement of science. BB Reports specifically appreciates receiving reports on: Negative results, Replication studies, Reanalysis of previous datasets.