<i>UBE2D1</i> promotes glioblastoma proliferation by modulating p21 ubiquitination-Reference-Cited by-同舟云学术

UBE2D1 promotes glioblastoma proliferation by modulating p21 ubiquitination

Published:2024-07-17 Issue:10 Volume:63 Page:1967-1979
ISSN:0899-1987
Container-title:Molecular Carcinogenesis
language:en
Short-container-title:Molecular Carcinogenesis

Author:

Wang Yongfeng¹,Ma Qianquan²,Li Haoyu³⁴,Huang Wei³⁴⁵,You Jia³⁴,Liu Dian⁶

Affiliation:

1. Department of Laboratory Medicine The First Affiliated Hospital of Zhengzhou University, Key Clinical Laboratory of Henan Province Zhengzhou China

2. Department of Neurosurgery, Peking University Third Hospital Peking University Beijing China

3. Department of Neurosurgery, Xiangya Hospital Central South University Changsha China

4. National Clinical Research Center for Geriatric Disorders, Xiangya Hospital Central South University Changsha China

5. Research Center of Carcinogenesis and Targeted Therapy, Xiangya Hospital Central South University Changsha China

6. Department of Lymphoma and Abdominal Radiotherapy, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine Central South University Changsha China

Abstract

AbstractGlioblastoma (GBM) cells exhibit aberrant proliferative abilities and resistance to conventional therapies. However, the mechanisms underlying these malignant phenotypes are poorly understood. In this study, we identified ubiquitin‐conjugating enzyme E2D1 (UBE2D1) as a crucial stimulator of GBM development. It is highly expressed in GBM and closely associated with poor prognosis in patients with GBM. UBE2D1 knockdown inhibits GBM cell growth and leads to G1 cell cycle arrest. Mechanistically, UBCH5A binds to p21 at the protein level and induces the ubiquitination and degradation of p21. This negative regulation is mediated by STUB1. Our findings are the first to identify UBE2D1 as a key driver of GBM growth and provide a potential target for improving prognosis and therapy.

Publisher

Wiley

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/mc.23786

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