Direct Effect of Bevacizumab on Glioblastoma Cell Lines In Vitro
| Autor: | Yusra Kassim, Elise Demange, Alexandre Petit, Valérie Perrot, Didier Le Cerf, Thomas Simon, Jean-Pierre Vannier, Bérénice Coquerel |
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| Přispěvatelé: | Micro-Environnement et Régulation Cellulaire Intégrée (MERCI), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU), Polymères Biopolymères Surfaces (PBS), Institut national des sciences appliquées Rouen Normandie (INSA Rouen Normandie), Institut National des Sciences Appliquées (INSA)-Normandie Université (NU)-Institut National des Sciences Appliquées (INSA)-Normandie Université (NU)-Institut de Chimie du CNRS (INC)-Institut Normand de Chimie Moléculaire Médicinale et Macromoléculaire (INC3M), Institut de Chimie du CNRS (INC)-École Nationale Supérieure d'Ingénieurs de Caen (ENSICAEN), Normandie Université (NU)-Normandie Université (NU)-Institut national des sciences appliquées Rouen Normandie (INSA Rouen Normandie), Institut National des Sciences Appliquées (INSA)-Normandie Université (NU)-Institut National des Sciences Appliquées (INSA)-Université Le Havre Normandie (ULH), Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS)-Université de Caen Normandie (UNICAEN), Normandie Université (NU)-École Nationale Supérieure d'Ingénieurs de Caen (ENSICAEN), Normandie Université (NU)-Université Le Havre Normandie (ULH), Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS) |
| Jazyk: | angličtina |
| Rok vydání: | 2014 |
| Předmět: |
Vascular Endothelial Growth Factor A
Pathology Indoles genetic structures Cell Culture Techniques Angiogenesis Inhibitors Pregnancy Proteins VEGF-A Anti-angiogenic therapies Brain extracellular matrix 0302 clinical medicine Cell Movement Sunitinib Neoplasm Hyaluronic Acid 0303 health sciences Brain Neoplasms Hydrogels [CHIM.MATE]Chemical Sciences/Material chemistry Neoplasm Proteins 3. Good health Bevacizumab Gene Expression Regulation Neoplastic Autocrine Communication Neurology 030220 oncology & carcinogenesis Monoclonal Molecular Medicine Cell Division Signal Transduction medicine.drug medicine.medical_specialty MAP Kinase Signaling System medicine.drug_class Antineoplastic Agents Antibodies Monoclonal Humanized Monoclonal antibody Autocrine loop 03 medical and health sciences Cellular and Molecular Neuroscience Cell Line Tumor medicine Humans Neoplasm Invasiveness Pyrroles Calcium Signaling Autocrine signalling Protein Kinase Inhibitors Protein kinase B Placenta Growth Factor 030304 developmental biology Vascular Endothelial Growth Factor Receptor-1 business.industry medicine.disease Vascular Endothelial Growth Factor Receptor-2 eye diseases nervous system diseases [CHIM.POLY]Chemical Sciences/Polymers Drug Resistance Neoplasm Cell culture Cancer research sense organs Drug Screening Assays Antitumor business Glioblastoma Proto-Oncogene Proteins c-akt |
| Zdroj: | NeuroMolecular Medicine NeuroMolecular Medicine, Humana Press, 2014, 16 (4), pp.752-771. ⟨10.1007/s12017-014-8324-8⟩ |
| ISSN: | 1535-1084 |
| DOI: | 10.1007/s12017-014-8324-8⟩ |
| Popis: | International audience; Bevacizumab is a humanized monoclonal antibody directed against the pro-angiogenic factor vascular and endothelial growth factor-A (VEGF-A) used in the treatment of glioblastomas. Although most patients respond initially to this treatment, studies have shown that glioblastomas eventually recur. Several non-mutually exclusive theories based on the anti-angiogenic effect of bevacizumab have been proposed to explain these mechanisms of resistance. In this report, we studied whether bevacizumab can act directly on malignant glioblastoma cells. We observe changes in the expression profiles of components of the VEGF/VEGF-R pathway and in the response to a VEGF-A stimulus following bevacizumab treatment. In addition, we show that bevacizumab itself acts on glioblastoma cells by activating the Akt and Erks survival signaling pathways. Bevacizumab also enhances proliferation and invasiveness of glioblastoma cells in hyaluronic acid hydrogel. We propose that the paradoxical effect of bevacizumab on glioblastoma cells could be due to changes in the VEGF-A-dependent autocrine loop as well as in the intracellular survival pathways, leading to the enhancement of tumor aggressiveness. Investigation of how bevacizumab interacts with glioblastoma cells and the resulting downstream signaling pathways will help targeting populations of resistant glioblastoma cells. |
| Databáze: | OpenAIRE |
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