Glioblastoma multiforme (GBM) is a commonly occurring brain tumor with a poor prognosis. GBM can develop both "de novo" or evolve from a previous astrocytoma and is characterized by high proliferation and infiltration into the surrounding tissue. Following treatment (surgery, radiotherapy, and chemotherapy), tumors often reappear. Glioma-initiating cells (GICs) have been identified in GBM and are thought to be responsible for tumors initiation, their continued growth, and recurrence. β-catenin, a component of the cell-cell adhesion complex and of the canonical Wnt pathway, regulates proliferation, adhesion, and migration in different cell types. β-catenin and components of the Wnt canonical pathway are commonly overexpressed in GBM. Here, we review previous work on the role of Wnt/β-catenin signalling in glioma initiation, proliferation, and invasion. Understanding the molecular mechanisms regulating GIC biology and glioma progression may help in identifying novel therapeutic targets for GBM treatment.
Keyphrases
- cell proliferation
- poor prognosis
- induced apoptosis
- epithelial mesenchymal transition
- cell adhesion
- stem cells
- signaling pathway
- cell cycle arrest
- long non coding rna
- single cell
- cell therapy
- minimally invasive
- pi k akt
- radiation therapy
- escherichia coli
- combination therapy
- endoplasmic reticulum stress
- pseudomonas aeruginosa
- cystic fibrosis
- mesenchymal stem cells
- acute coronary syndrome
- staphylococcus aureus
- radiation induced
- atrial fibrillation
- replacement therapy
- chemotherapy induced