CLIC1 regulation of cancer stem cells in glioblastoma.
Angiogenesis
Cancer stem cells
Chloride intracellular channel 1
Glioblastoma
Invasion
Migration
Proliferation
Reactive oxygen species
Self-renewal
Journal
Current topics in membranes
ISSN: 1063-5823
Titre abrégé: Curr Top Membr
Pays: United States
ID NLM: 9212591
Informations de publication
Date de publication:
2023
2023
Historique:
medline:
27
11
2023
pubmed:
26
11
2023
entrez:
25
11
2023
Statut:
ppublish
Résumé
Chloride intracellular channel 1 (CLIC1) has emerged as a therapeutic target in various cancers. CLIC1 promotes cell cycle progression and cancer stem cell (CSC) self-renewal. Furthermore, CLIC1 is shown to play diverse roles in proliferation, cell volume regulation, tumour invasion, migration, and angiogenesis. In glioblastoma (GB), CLIC1 facilitates the G1/S phase transition and tightly regulates glioma stem-like cells (GSCs), a rare population of self-renewing CSCs with central roles in tumour resistance to therapy and tumour recurrence. CLIC1 is found as either a monomeric soluble protein or as a non-covalent dimeric protein that can form an ion channel. The ratio of dimeric to monomeric protein is altered in GSCs and depends on the cell redox state. Elucidating the mechanisms underlying the alterations in CLIC1 expression and structural transitions will further our understanding of its role in GSC biology. This review will highlight the role of CLIC1 in GSCs and its significance in facilitating different hallmarks of cancer.
Identifiants
pubmed: 38007271
pii: S1063-5823(23)00025-X
doi: 10.1016/bs.ctm.2023.09.004
pii:
doi:
Substances chimiques
Chloride Channels
0
CLIC1 protein, human
0
Types de publication
Review
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
99-123Informations de copyright
Copyright © 2023. Published by Elsevier Inc.