Astrocyte elevated gene-1 as a novel therapeutic target in malignant gliomas and its interactions with oncogenes and tumor suppressor genes.


Journal

Brain research
ISSN: 1872-6240
Titre abrégé: Brain Res
Pays: Netherlands
ID NLM: 0045503

Informations de publication

Date de publication:
15 11 2020
Historique:
received: 01 06 2020
revised: 19 07 2020
accepted: 25 07 2020
pubmed: 4 8 2020
medline: 8 10 2021
entrez: 4 8 2020
Statut: ppublish

Résumé

Astrocyte elevated gene-1 (AEG-1) is an oncogene and a critical signaling molecule that has a wide variety of interactions with other oncogenes and tumor suppressor genes, leading to increasing malignant properties of malignant gliomas, such as invasion, angiogenesis, metastasis, and chemoresistance. Its overexpression is enhanced by many factors such as exposure of the cells to human immunodeficiency virus type 1 (HIV-1), HIV-1 envelop glycoprotein 120, hypoxia, or glucose deprivation. Thorough understanding of these interactions along with AEG-1 inducers and repressors is important in setting a successful treatment plan targeting this oncogene. Since its discovery in 2002, AEG-1 has made a significant impact in improving our understanding of mechanism of malignant tumors progression, such as breast carcinomas, melanoma, and malignant gliomas. Therefore, it has been a novel therapeutic target for the past two decades. Herein, we focus on the role of AEG-1 in malignant gliomas and its interaction with other signaling molecules.

Identifiants

pubmed: 32745657
pii: S0006-8993(20)30390-5
doi: 10.1016/j.brainres.2020.147034
pii:
doi:

Substances chimiques

Antineoplastic Agents 0
MTDH protein, human 0
Membrane Proteins 0
RNA-Binding Proteins 0

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

147034

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

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

Mahmoud Osama (M)

Faculty of Medicine, Zagazig University, Zagazig, Egypt. Electronic address: mahmoud216498@medicine.zu.edu.eg.

Mostafa Nasr Mostafa (MN)

Faculty of Medicine, Zagazig University, Zagazig, Egypt.

Mohammed Ali Alvi (MA)

Mayo Clinic Neuro-Informatics Laboratory, Mayo Clinic, Rochester, MN, USA.

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Classifications MeSH