Table of Contents
Chemotherapy Research and Practice
Volume 2012 (2012), Article ID 192362, 7 pages
http://dx.doi.org/10.1155/2012/192362
Review Article

β-Catenin Signalling in Glioblastoma Multiforme and Glioma-Initiating Cells

1Departments of Basic Medical Sciences and Experimental Medicine, IRBLleida University of Lleida, 25198 Lleida, Spain
2Neurosurgery Unit, University Hospital Arnau de Vilanova, 25198 Lleida, Spain

Received 19 April 2011; Revised 23 November 2011; Accepted 24 November 2011

Academic Editor: Paolo Pronzato

Copyright © 2012 Mireia Nager et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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.