The cytoskeleton and brain tumour cell migration.
Although the mechanics of brain tumour cell motility are poorly documented, studies in other cell types-notably fibroblasts--have revealed cell motility to be dependent on dynamic remodelling of the actin cytoskeleton. Initially, protrusion of membrane microspikes or lamellipodia is associated with actin polymerisation and probably involves membrane-anchored myosin I. Subsequent attachment of the cell's leading edge to the substratum is via actin-anchored adhesion complexes and finally generation of tractile forces is believed to involve the formation of contractile actin structures. Co-ordination of these events is even less well understood but recent evidence points to the involvement of the Ras family of GTP-binding proteins, particularly the cdc42-Rac-Rho cascade which appears to choreograph membrane extension and attachment. Furthermore, the growth associated protein GAP-43 (neuromodulin) has recently been demonstrated in brain tumour cells. This protein stabilises membrane protrusions during neuritogenesis in response to external trophic factors and is likely to have a similar role in brain tumour cell invasion.
Maidment
S L
SL
Department of Neuropathology, Institute of Psychiatry, London, U.K.
D000199:Actins / Q000502:physiology*; D000818:Animals; D001932:Brain Neoplasms / Q000473:pathology / Q000503:physiopathology*; D002448:Cell Adhesion / Q000502:physiology*; D002465:Cell Movement / Q000502:physiology*; D003599:Cytoskeleton / Q000502:physiology*; D004023:Dictyostelium; D005910:Glioma / Q000503:physiopathology; D006801:Humans
D000199:Actins