Role of PLCγ1 in the modulation of cell migration and cell invasion in glioblastoma.
Biomarker
Glioblastoma
Invasion
Migration
Overexpression
PLCγ1
Silencing
Journal
Advances in biological regulation
ISSN: 2212-4934
Titre abrégé: Adv Biol Regul
Pays: England
ID NLM: 101572336
Informations de publication
Date de publication:
01 2022
01 2022
Historique:
received:
02
11
2021
revised:
12
11
2021
accepted:
16
11
2021
pubmed:
26
11
2021
medline:
6
4
2022
entrez:
25
11
2021
Statut:
ppublish
Résumé
Phosphoinositide-specific phospholipases C (PLCs) are a class of enzymes involved in several cell activities, such as cell cycle regulation, proliferation, differentiation and cytoskeletal dynamics. Among these enzymes, PLCγ1 is one of the most expressed PLCs in the brain, contributing to a complex network in the developing nervous system. Several studies have shown that PLCγ1 signaling imbalance is linked to several brain disorders, including glioblastoma, the most aggressive brain tumor in adults. Indeed, it has been demonstrated a link between PLCγ1 inhibition and the arrest of glioma cell motility of fetal rat brain aggregates and the impairment of cell invasion abilities following its down-regulation. This study aims to determine the pathological influence of PLCγ1 in glioblastoma, through a translational study which combines in silico data, data from glioblastoma patients' samples and data on engineered cell lines. We found out that PLCγ1 gene expression correlates with the pathological grade of gliomas, and it is higher in fifty patients' glioblastoma tissue samples compared to twenty healthy controls. Moreover, it was demonstrated that PLCγ1 silencing in U87-MG leads to a reduction in cell migration and invasion abilities. The opposite trend was observed following PLCγ1 overexpression, suggesting an interesting possible involvement of PLCγ1 in gliomas' aggressiveness.
Identifiants
pubmed: 34819252
pii: S2212-4926(21)00054-3
doi: 10.1016/j.jbior.2021.100838
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
100838Informations de copyright
Copyright © 2021 Elsevier Ltd. All rights reserved.