The Neural Extracellular Matrix, Cell Adhesion Molecules and Proteolysis in Glioma Invasion and Tumorigenicity

摘要: High-grade gliomas are the most prevalent and lethal form of primary intracranial tumors. Despite significant progress in surgical adjuvant therapeutic treatments for gliomas, patient prognosis still remains dismal. The ability to invade normal surrounding brain tissue contributes their capacity evade interventions, ultimately leading tumor recurrence subsequent disease progression (Rich & Bigner, 2004). Another major obstacle comes from high degree intratumoral cellular heterogeneity. mass is comprised both terminally differentiated cells, cells that exhibit finite capabilities self-renewal multipotency, a smaller subpopulation stem cell-like qualities. These stem-like termed Glioma Initiating Cells (GICs), exihibit pluripotency, and, importantly, capable repopulating original parental tumor. Therefore, more effective therapies may be derived targeting infiltrative nature GICs (Louis, 2006; Park Rich, 2009). glioma infiltrate property restricted tumors phenotypically glial within central nervous system (CNS). As metastatic highly invasive periphery fail once confines CNS, originate rarely metastasize outside CNS. findings suggest unique interaction between neural extracellular environment mediate invasion (Bellail et al., 2004; Nutt 2001a). A defining attribute composition matrix (ECM), which unlike other peripheral matrices has low levels fibrilliar proteins like collagens, fibronectin, laminin (Ruoslahti, 1996). In development pathogenesis, ECM regulates key biological processes including migration, maturation, synapse formation, plasticity. adult largely inhibitory reorganization (Galtrey Fawcett, 2007; Zimmermann Dours-Zimmermann, 2008). cell into overcome this normally environment. Decades research