Serglycin activates pro-tumorigenic signaling and controls glioblastoma cell stemness, differentiation and invasive potential.
ALDH1, aldehyde dehydrogenase 1
Astrocytic differentiation
CXCR, C-X-C chemokine receptor
ECM, extracellular matrix
EMT, epithelial to mesenchymal transition
ERK, extracellular-signal-regulated kinase
GFAP, glial fibrillary acid protein
Glioblastoma
IL, interleukin
Interleukins
MAPK, mitogen-activated protein kinase
MMPs, metalloproteinases
PGs, proteoglycans
PI3K, phosphoinositide 3-kinase
Proteoglycans
Proteolytic enzymes
SRGN, serglycin
STAT-3, signal transducer and activator of transcription 3
Serglycin
Signaling
Stemness
TIMPs, tissue inhibitors of metalloproteinases
uPA, urokinase plasminogen activator
Journal
Matrix biology plus
ISSN: 2590-0285
Titre abrégé: Matrix Biol Plus
Pays: Netherlands
ID NLM: 101775320
Informations de publication
Date de publication:
May 2020
May 2020
Historique:
received:
03
12
2019
revised:
06
03
2020
accepted:
06
03
2020
entrez:
5
2
2021
pubmed:
6
2
2021
medline:
6
2
2021
Statut:
epublish
Résumé
Despite the functional role of serglycin as an intracellular proteoglycan, a variety of malignant cells depends on its expression and constitutive secretion to advance their aggressive behavior. Serglycin arose to be a biomarker for glioblastoma, which is the deadliest and most treatment-resistant form of brain tumor, but its role in this disease is not fully elucidated. In our study we suppressed the endogenous levels of serglycin in LN-18 glioblastoma cells to decipher its involvement in their malignant phenotype. Serglycin suppressed LN-18 (LN-18
Identifiants
pubmed: 33543029
doi: 10.1016/j.mbplus.2020.100033
pii: S2590-0285(20)30014-4
pmc: PMC7852318
doi:
Types de publication
Journal Article
Langues
eng
Pagination
100033Informations de copyright
© 2020 The Authors.
Déclaration de conflit d'intérêts
The authors declare that no conflict of interest exists.
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