Glioblastoma multiforme (GBM) is the most aggressive malignant tumor of the central nervous system, with poor survival in both treated and untreated patients. Recent studies began to explain the molecular pathway, comprising the dynamic structural and mechanical changes involved in GBM. In this context, some studies showed that the human glioblastoma cells release high levels of glutamate, which regulates the proliferation and survival of neuronal progenitor cells. Considering that cancer cells possess properties in common with neural progenitor cells, it is likely that the functions of glutamate receptors may affect the growth of cancer cells and, therefore, open the road to new and more targeted therapies.
Keywords: N-methyl-d-aspartate (NMDA); cell migration; focal adhesion complex (FAK); glioblastoma multiforme; glutamate receptors; mechanobiology; protein kinase B (Akt); α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA).