Glioblastoma Factors Increase the Migration of Human Brain Endothelial Cells
Brain
/ pathology
Brain Neoplasms
/ genetics
Cell Movement
/ drug effects
Cell Proliferation
/ drug effects
Chemokine CXCL12
/ metabolism
Culture Media, Conditioned
/ pharmacology
Endothelial Cells
/ drug effects
Gene Expression Regulation, Neoplastic
/ drug effects
Glioblastoma
/ genetics
Humans
Matrix Metalloproteinase 9
/ metabolism
RNA, Messenger
/ genetics
Receptors, CXCR
/ metabolism
Receptors, CXCR4
/ metabolism
Vascular Endothelial Growth Factor A
/ metabolism
Vascular Endothelial Growth Factor Receptor-2
/ metabolism
Wnt-5a Protein
/ genetics
Angiogenesis
CXCR4
MMP-9
cell crosstalk
endothelial cells
glioblastoma
Journal
Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988
Informations de publication
Date de publication:
May 2020
May 2020
Historique:
received:
18
03
2020
revised:
30
03
2020
accepted:
31
03
2020
entrez:
6
5
2020
pubmed:
6
5
2020
medline:
15
5
2020
Statut:
ppublish
Résumé
Glioblastoma (GB) is the most aggressive type of tumor in the central nervous system and is characterized by resistance to therapy and abundant vasculature. Tumor vessels contribute to the growth of GB, and the tumor microenvironment is thought to influence tumor vessels. We evaluated the molecular communication between human GB cells and human brain microvascular endothelial cells (HBMEC) in vitro. We investigated whether GB-conditioned media (GB-CM) influenced HBMEC proliferation and migration, as well as the levels of MMP-9, CXCL12, CXCR4, CXCR7, VEGFs, VEGFR-2, and WNT5a in HBMEC. Although HBMEC proliferation was not modified, increased HBMEC migration was detected after GB-CM treatment. Furthermore, treatment of HBMEC with GB-CM resulted in increased levels of MMP-9 and CXCR4. The levels of WNT5a, VEGFs and VEGFR-2 were not affected. GB-secreted factors lead to increased endothelial cell migration and to increased levels of MMP-9 and CXCR4.
Sections du résumé
BACKGROUND/AIM
OBJECTIVE
Glioblastoma (GB) is the most aggressive type of tumor in the central nervous system and is characterized by resistance to therapy and abundant vasculature. Tumor vessels contribute to the growth of GB, and the tumor microenvironment is thought to influence tumor vessels. We evaluated the molecular communication between human GB cells and human brain microvascular endothelial cells (HBMEC) in vitro.
MATERIALS AND METHODS
METHODS
We investigated whether GB-conditioned media (GB-CM) influenced HBMEC proliferation and migration, as well as the levels of MMP-9, CXCL12, CXCR4, CXCR7, VEGFs, VEGFR-2, and WNT5a in HBMEC.
RESULTS
RESULTS
Although HBMEC proliferation was not modified, increased HBMEC migration was detected after GB-CM treatment. Furthermore, treatment of HBMEC with GB-CM resulted in increased levels of MMP-9 and CXCR4. The levels of WNT5a, VEGFs and VEGFR-2 were not affected.
CONCLUSION
CONCLUSIONS
GB-secreted factors lead to increased endothelial cell migration and to increased levels of MMP-9 and CXCR4.
Identifiants
pubmed: 32366418
pii: 40/5/2725
doi: 10.21873/anticanres.14244
doi:
Substances chimiques
ACKR3 protein, human
0
CXCR4 protein, human
0
Chemokine CXCL12
0
Culture Media, Conditioned
0
RNA, Messenger
0
Receptors, CXCR
0
Receptors, CXCR4
0
Vascular Endothelial Growth Factor A
0
Wnt-5a Protein
0
Vascular Endothelial Growth Factor Receptor-2
EC 2.7.10.1
Matrix Metalloproteinase 9
EC 3.4.24.35
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2725-2737Informations de copyright
Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.