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

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 li...

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Main Authors: Zi-Long Wei, Shuo Han, Dong-Hua Han, Xue-Tao Li, Yu-Lun Huang, Zhi-Min Wang
Format: Article
Language:English
Published: Elsevier 2025-06-01
Series:Biochemistry and Biophysics Reports
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Online Access:http://www.sciencedirect.com/science/article/pii/S2405580825001359
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author Zi-Long Wei
Shuo Han
Dong-Hua Han
Xue-Tao Li
Yu-Lun Huang
Zhi-Min Wang
author_facet Zi-Long Wei
Shuo Han
Dong-Hua Han
Xue-Tao Li
Yu-Lun Huang
Zhi-Min Wang
author_sort Zi-Long Wei
collection DOAJ
description 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.
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series Biochemistry and Biophysics Reports
spelling doaj-art-761e22d5f5724ca8a3df70abbdfa2a322025-08-20T02:37:46ZengElsevierBiochemistry and Biophysics Reports2405-58082025-06-014210204810.1016/j.bbrep.2025.102048β-suppressor protein 1 (ARRB1)-△exon13 modulates the progression of glioblastoma via combination with glycolysis-related proteinsZi-Long Wei0Shuo Han1Dong-Hua Han2Xue-Tao Li3Yu-Lun Huang4Zhi-Min Wang5Department of Neurosurgery, The Fourth Hospital Affiliated to Soochow University, Suzhou Dushu Lake Hospital, Suzhou, 215000, China; Department of Neurosurgery, Shanghai Pudong Hospital Affliated to Fudan University, Pudong Medical Center, Shanghai, 201399, ChinaDepartment of Neurosurgery, Shanghai Changzheng Hospital, Shanghai, ChinaDepartment of Neurosurgery, Shanghai Pudong Hospital Affliated to Fudan University, Pudong Medical Center, Shanghai, 201399, ChinaDepartment of Neurosurgery, The Fourth Hospital Affiliated to Soochow University, Suzhou Dushu Lake Hospital, Suzhou, 215000, ChinaDepartment of Neurosurgery, The Fourth Hospital Affiliated to Soochow University, Suzhou Dushu Lake Hospital, Suzhou, 215000, ChinaDepartment of Neurosurgery, The Fourth Hospital Affiliated to Soochow University, Suzhou Dushu Lake Hospital, Suzhou, 215000, China; Corresponding author. No. 9 Chongwen Road, Suzhou Industrial Park, Jiangsu, China.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.http://www.sciencedirect.com/science/article/pii/S2405580825001359GlioblastomaARRB1Alternative spicingGlycolysisMalignancy
spellingShingle Zi-Long Wei
Shuo Han
Dong-Hua Han
Xue-Tao Li
Yu-Lun Huang
Zhi-Min Wang
β-suppressor protein 1 (ARRB1)-△exon13 modulates the progression of glioblastoma via combination with glycolysis-related proteins
Biochemistry and Biophysics Reports
Glioblastoma
ARRB1
Alternative spicing
Glycolysis
Malignancy
title β-suppressor protein 1 (ARRB1)-△exon13 modulates the progression of glioblastoma via combination with glycolysis-related proteins
title_full β-suppressor protein 1 (ARRB1)-△exon13 modulates the progression of glioblastoma via combination with glycolysis-related proteins
title_fullStr β-suppressor protein 1 (ARRB1)-△exon13 modulates the progression of glioblastoma via combination with glycolysis-related proteins
title_full_unstemmed β-suppressor protein 1 (ARRB1)-△exon13 modulates the progression of glioblastoma via combination with glycolysis-related proteins
title_short β-suppressor protein 1 (ARRB1)-△exon13 modulates the progression of glioblastoma via combination with glycolysis-related proteins
title_sort β suppressor protein 1 arrb1 △exon13 modulates the progression of glioblastoma via combination with glycolysis related proteins
topic Glioblastoma
ARRB1
Alternative spicing
Glycolysis
Malignancy
url http://www.sciencedirect.com/science/article/pii/S2405580825001359
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