1. Glioblastoma Factors Increase the Migration of Human Brain Endothelial Cells In Vitro by Increasing MMP-9/CXCR4 Levels.
- Author
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DE Oliveira Rosario LV, DA Rosa BG, Goncalves TL, Matias DIL, Freitas C, and Ferrer VP
- Subjects
- Brain Neoplasms genetics, Cell Proliferation drug effects, Chemokine CXCL12 metabolism, Culture Media, Conditioned pharmacology, Endothelial Cells drug effects, Gene Expression Regulation, Neoplastic drug effects, Glioblastoma genetics, Humans, RNA, Messenger genetics, RNA, Messenger metabolism, Receptors, CXCR metabolism, Vascular Endothelial Growth Factor A metabolism, Vascular Endothelial Growth Factor Receptor-2 metabolism, Wnt-5a Protein genetics, Wnt-5a Protein metabolism, Brain pathology, Brain Neoplasms pathology, Cell Movement drug effects, Endothelial Cells pathology, Glioblastoma pathology, Matrix Metalloproteinase 9 metabolism, Receptors, CXCR4 metabolism
- Abstract
Background/aim: 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: 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: 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: GB-secreted factors lead to increased endothelial cell migration and to increased levels of MMP-9 and CXCR4., (Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)
- Published
- 2020
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