Publication Date
1-1-2023
Journal
International Journal of Molecular Sciences
DOI
10.3390/ijms24010749
PMID
36614191
PMCID
PMC9820922
PubMedCentral® Posted Date
1-1-2023
PubMedCentral® Full Text Version
Post-print
Published Open-Access
yes
Keywords
Humans, Glioblastoma, Neurons, Synapses, Nervous System Physiological Phenomena, Signal Transduction, Cell Adhesion Molecules, Neuronal, glioma, glioblastoma, tumor microenvironment, hyperexcitability, neuroglial synapse, glutamate, neuroligin-3
Abstract
Glioblastoma is the most common malignant primary brain tumor. Recent studies have demonstrated that excitatory or activity-dependent signaling-both synaptic and non-synaptic-contribute to the progression of glioblastoma. Glutamatergic receptors may be stimulated via neuron-tumor synapses or release of glutamate by the tumor itself. Ion currents generated by these receptors directly alter the structure of membrane adhesion molecules and cytoskeletal proteins to promote migratory behavior. Additionally, the hyperexcitable milieu surrounding glioma increases the rate at which tumor cells proliferate and drive recurrent disease. Inhibition of excitatory signaling has shown to effectively reduce its pro-migratory and -proliferative effects.