G6PD drives glioma invasion by regulating SQSTM1 protein stability.


Journal

Gene
ISSN: 1879-0038
Titre abrégé: Gene
Pays: Netherlands
ID NLM: 7706761

Informations de publication

Date de publication:
20 Jul 2023
Historique:
received: 28 02 2023
revised: 20 04 2023
accepted: 05 05 2023
medline: 9 6 2023
pubmed: 16 5 2023
entrez: 15 5 2023
Statut: ppublish

Résumé

Glioma is an incurable brain tumor with high recurrence due to the frequent invasion of neoplastic cells. Glucose-6-phosphate dehydrogenase (G6PD) is a critical enzyme in the pentose phosphate pathway (PPP) whose aberrant expression drives the pathogenesis of various cancers. Recent research has identified other moonlight modes of enzymes besides the well-known regulation of metabolic reprogramming. Here, we identified previously unexplored roles of G6PD in glioma via gene set variation analysis (GSVA) based on the Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA) database. Furthermore, survival analyses revealed that glioma patients with high G6PD expression had a worse outcome than patients with low G6PD expression (Hazard Ratio (95%CI): 2.96 (2.41, 3.64), p = 3.5E-22). Combined with functional assays, G6PD was shown to be related with the migration and invasion in glioma. G6PD knockdown could inhibit the migration in LN229 cells. And G6PD overexpression enhanced LN229 cell migration and invasion. Mechanically, the knockdown of G6PD reduced sequestosome 1 (SQSTM1) protein stability under cycloheximide (CHX) treatment. Moreover, the overexpression of SQSTM1 rescued the impaired migrated and invasive phenotypes in G6PD-silenced cells. Clinically, we validated the role of G6PD-SQSTM1 axis in glioma prognosis by constructing the multivariate cox proportional hazards regression model. These results define a pivotal function of G6PD in modulating SQSTM1 to promote glioma aggressiveness. And G6PD may be a prognostic biomarker and potential therapeutic target in glioma. G6PD-SQSTM1 axis may be a potential prognostic biomarker in glioma.

Identifiants

pubmed: 37187243
pii: S0378-1119(23)00317-7
doi: 10.1016/j.gene.2023.147476
pii:
doi:

Substances chimiques

Glucosephosphate Dehydrogenase EC 1.1.1.49
Sequestosome-1 Protein 0
Biomarkers 0
SQSTM1 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

147476

Informations de copyright

Copyright © 2023. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Xin Zhang (X)

State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences, Medical Primate Research Center, Neuroscience Center, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.

Zhixing Wang (Z)

State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences, Medical Primate Research Center, Neuroscience Center, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.

Rui Zhuo (R)

State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences, Medical Primate Research Center, Neuroscience Center, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.

Liping Wang (L)

State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences, Medical Primate Research Center, Neuroscience Center, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.

Yiming Qin (Y)

State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences, Medical Primate Research Center, Neuroscience Center, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China.

Wei Han (W)

State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences, Medical Primate Research Center, Neuroscience Center, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China. Electronic address: hanwei2012@ibms.pumc.edu.cn.

Xiaozhong Peng (X)

State Key Laboratory of Medical Molecular Biology, Department of Molecular Biology and Biochemistry, Institute of Basic Medical Sciences, Medical Primate Research Center, Neuroscience Center, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing 100005, China; National Human Diseases Animal Model Resource Center, Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases, Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences & Peking Union Medical College , Beijing 100021, China. Electronic address: pengxiaozhong@pumc.edu.cn.

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