TSPYL5-driven G3BP1 nuclear membrane translocation facilitates p53 cytoplasm sequestration via accelerating RanBP2-mediated p53 sumoylation and nuclear export in neuroblastoma

Abstract Cytoplasmic sequestration of wild-type p53, representing a nonmutational event of p53 activity suppression, is a characteristic phenotype of undifferentiated neuroblastoma (NB); however, the underlying mechanism is yet to be defined. In the present study, we observed that TSPYL5 effectively...

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Main Authors: Zhaokun Wang, Yunqiang Liu, Yangwei Zhang, Jiaying Shi, Shengyu Xie, Ming Yi, Xinyue Zhang, Dachang Tao, Yuan Yang
Format: Article
Language:English
Published: Nature Publishing Group 2025-05-01
Series:Cell Death and Disease
Online Access:https://doi.org/10.1038/s41419-025-07694-x
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author Zhaokun Wang
Yunqiang Liu
Yangwei Zhang
Jiaying Shi
Shengyu Xie
Ming Yi
Xinyue Zhang
Dachang Tao
Yuan Yang
author_facet Zhaokun Wang
Yunqiang Liu
Yangwei Zhang
Jiaying Shi
Shengyu Xie
Ming Yi
Xinyue Zhang
Dachang Tao
Yuan Yang
author_sort Zhaokun Wang
collection DOAJ
description Abstract Cytoplasmic sequestration of wild-type p53, representing a nonmutational event of p53 activity suppression, is a characteristic phenotype of undifferentiated neuroblastoma (NB); however, the underlying mechanism is yet to be defined. In the present study, we observed that TSPYL5 effectively tethers p53 in the cytoplasm and greatly inhibits its function as a transcription factor. Mechanistically, the binding of TSPYL5 with G3BP1 enhances G3BP1 Ser149 phosphorylation to drive G3BP1 nuclear membrane translocation, which recruits more p53 for nucleoporin RanBP2 by the formation of the RanBP2-G3BP1-p53 complex. Thus, the accelerating p53 sumoylation promotes its nuclear export. With this signal pathway, TSPYL5 augments the malignant characteristics of neuroblastoma cells. Our findings unravel a detailed TSPYL5-driven molecular axis that sheds light on the regulating system of the p53 sumoylation-based cytoplasmic sequestration in NB cells, paving the way for the novel therapeutic opportunities for NB cancers by antagonizing TSPYL5 function.
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issn 2041-4889
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publisher Nature Publishing Group
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series Cell Death and Disease
spelling doaj-art-2b9f8691239d4d418ef8154606e69c472025-08-20T02:10:53ZengNature Publishing GroupCell Death and Disease2041-48892025-05-0116111310.1038/s41419-025-07694-xTSPYL5-driven G3BP1 nuclear membrane translocation facilitates p53 cytoplasm sequestration via accelerating RanBP2-mediated p53 sumoylation and nuclear export in neuroblastomaZhaokun Wang0Yunqiang Liu1Yangwei Zhang2Jiaying Shi3Shengyu Xie4Ming Yi5Xinyue Zhang6Dachang Tao7Yuan Yang8Department of Medical Genetics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan UniversityDepartment of Medical Genetics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan UniversityDepartment of Medical Genetics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan UniversityDepartment of Medical Genetics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan UniversityDepartment of Medical Genetics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan UniversityDepartment of Medical Genetics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan UniversityDepartment of Medical Genetics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan UniversityDepartment of Medical Genetics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan UniversityDepartment of Medical Genetics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan UniversityAbstract Cytoplasmic sequestration of wild-type p53, representing a nonmutational event of p53 activity suppression, is a characteristic phenotype of undifferentiated neuroblastoma (NB); however, the underlying mechanism is yet to be defined. In the present study, we observed that TSPYL5 effectively tethers p53 in the cytoplasm and greatly inhibits its function as a transcription factor. Mechanistically, the binding of TSPYL5 with G3BP1 enhances G3BP1 Ser149 phosphorylation to drive G3BP1 nuclear membrane translocation, which recruits more p53 for nucleoporin RanBP2 by the formation of the RanBP2-G3BP1-p53 complex. Thus, the accelerating p53 sumoylation promotes its nuclear export. With this signal pathway, TSPYL5 augments the malignant characteristics of neuroblastoma cells. Our findings unravel a detailed TSPYL5-driven molecular axis that sheds light on the regulating system of the p53 sumoylation-based cytoplasmic sequestration in NB cells, paving the way for the novel therapeutic opportunities for NB cancers by antagonizing TSPYL5 function.https://doi.org/10.1038/s41419-025-07694-x
spellingShingle Zhaokun Wang
Yunqiang Liu
Yangwei Zhang
Jiaying Shi
Shengyu Xie
Ming Yi
Xinyue Zhang
Dachang Tao
Yuan Yang
TSPYL5-driven G3BP1 nuclear membrane translocation facilitates p53 cytoplasm sequestration via accelerating RanBP2-mediated p53 sumoylation and nuclear export in neuroblastoma
Cell Death and Disease
title TSPYL5-driven G3BP1 nuclear membrane translocation facilitates p53 cytoplasm sequestration via accelerating RanBP2-mediated p53 sumoylation and nuclear export in neuroblastoma
title_full TSPYL5-driven G3BP1 nuclear membrane translocation facilitates p53 cytoplasm sequestration via accelerating RanBP2-mediated p53 sumoylation and nuclear export in neuroblastoma
title_fullStr TSPYL5-driven G3BP1 nuclear membrane translocation facilitates p53 cytoplasm sequestration via accelerating RanBP2-mediated p53 sumoylation and nuclear export in neuroblastoma
title_full_unstemmed TSPYL5-driven G3BP1 nuclear membrane translocation facilitates p53 cytoplasm sequestration via accelerating RanBP2-mediated p53 sumoylation and nuclear export in neuroblastoma
title_short TSPYL5-driven G3BP1 nuclear membrane translocation facilitates p53 cytoplasm sequestration via accelerating RanBP2-mediated p53 sumoylation and nuclear export in neuroblastoma
title_sort tspyl5 driven g3bp1 nuclear membrane translocation facilitates p53 cytoplasm sequestration via accelerating ranbp2 mediated p53 sumoylation and nuclear export in neuroblastoma
url https://doi.org/10.1038/s41419-025-07694-x
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