Maidment S L
Department of Neuropathology, Institute of Psychiatry, London, U.K.
Anticancer Res. 1997 Nov-Dec;17(6B):4145-9.
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.
尽管脑肿瘤细胞运动的机制鲜有文献记载，但对其他细胞类型（尤其是成纤维细胞）的研究表明，细胞运动依赖于肌动蛋白细胞骨架的动态重塑。最初，膜微刺或片状伪足的突出与肌动蛋白聚合有关，可能涉及膜锚定的肌球蛋白I。细胞前沿随后通过肌动蛋白锚定的黏附复合物附着于基质，最后据信牵张力的产生涉及收缩性肌动蛋白结构的形成。这些事件的协调机制更是鲜为人知，但最近的证据表明，GTP结合蛋白的Ras家族参与其中，特别是cdc42-Rac-Rho级联反应，它似乎在编排膜的延伸和附着过程。此外，最近在脑肿瘤细胞中发现了生长相关蛋白GAP-43（神经调节蛋白）。这种蛋白在神经突发生过程中响应外部营养因子时稳定膜突出，并且可能在脑肿瘤细胞侵袭中发挥类似作用。
