Molecular approaches to brain tumour invasion.
In glioma cells, the stimulatory input of extracellular matrix components and an increased sensitivity to growth factors result in a high proliferative and migratory behaviour. Cell surface receptor interactions play pivotal roles in converging information about conditions in the environment immediately outside the cell. The transduced signal, in turn induces a response within the cell that provokes a specific behaviour. Cellular migration and cell proliferation are interwoven processes that share several common intracellular pathways. The major cross-links are the phosphoinositol phosphate regulating enzymes, PI-3 kinase and PTEN, the focal adhesion kinase (FAK) and the tumour suppressor p53. An understanding of the interaction between the molecular participants involved in migration and proliferation will promote the design of new treatments. A full understanding of the basis of the invasiveness of tumour cells remains elusive. Gene and protein expression are being studied, using modern techniques such as microarray analysis, SAGE and 2-D protein gels. Transient and permanent protein-protein interactions and recruitment of proteins to specialised cellular domains are equally important in regulating cellular invasion and presumably will attract more attention in future.
Günther
W
W
Department of Neurosurgery, Medical University of Lubeck, Germany.
Skaftnesmo
K-O
KO
Arnold
H
H
Terzis
A J A
AJ
D000818:Animals; D001932:Brain Neoplasms / Q000235:genetics* / Q000473:pathology; D002455:Cell Division / Q000235:genetics; D002465:Cell Movement / Q000235:genetics; D016326:Extracellular Matrix Proteins / Q000235:genetics; D051417:Focal Adhesion Kinase 1; D051416:Focal Adhesion Protein-Tyrosine Kinases; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology; D016158:Genes, p53 / Q000235:genetics; D005910:Glioma / Q000235:genetics* / Q000473:pathology; D006133:Growth Substances / Q000235:genetics; D006801:Humans; D009361:Neoplasm Invasiveness / Q000235:genetics* / Q000473:pathology; D051059:PTEN Phosphohydrolase; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics; D010744:Phosphoric Monoester Hydrolases / Q000235:genetics; D011505:Protein-Tyrosine Kinases / Q000235:genetics; D015398:Signal Transduction / Q000235:genetics; D025521:Tumor Suppressor Proteins / Q000235:genetics
D016326:Extracellular Matrix Proteins; D006133:Growth Substances; D025521:Tumor Suppressor Proteins; D019869:Phosphatidylinositol 3-Kinases; D011505:Protein-Tyrosine Kinases; D051417:Focal Adhesion Kinase 1; D051416:Focal Adhesion Protein-Tyrosine Kinases; C496050:PTK2 protein, human; D010744:Phosphoric Monoester Hydrolases; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human