癌细胞运动与迁移的分子机制

癌细胞运动和迁移的分子机制远较我们想象的复杂，癌细胞的运动和迁移性和接触性刺激相应答的细胞膜突起形成所启动的多步骤过程的结果.人们普遍想相信,片状伪足在驱动癌细胞迁移中起着主要作用,它通过附着在基底膜上而产生拉动细胞体向前的力量.近来的研究证明,切丝蛋白是癌细胞运动和迁移的一个重要调节因子, 切丝蛋白的局部激活可以诱导片状伪足的形成,并设定细胞运动方向.此外,成束蛋白.Arp2/3复合物、Cdc42、LIM激酶和黏着斑激酶常常协同调节癌细胞的运动和迁移.虽然调节癌细胞运动和迁移的信号通路和分子机制尚未完全阐明,但现有的资料清楚地表明,抑制癌细胞的迁移性将可能成为抑制恶性肿瘤生长和扩散的一个有用的策略.

Advances in Mechanisms of Cancer Cell Motility and Migration

The molecular mechanisms of cancer cell motility and migration is more complicated than that expected .The motility and migration of cancer cell is the result of multi-step processes initiated by the formation of membrane protrusions in response to migratory and chemotactic stimuli.It is generally believed that lamellipodia have a major role in driving cancer cell migration by attaching to the substrate and generating force to pull the cell body forward. Recent studies demonstrated that cofilin is an essential regulator of cancer cell motility and migration, local activation of cofilin may induce lamellipodia formation and set the direction of cell motility. In addition, fascin, Arp2/3 complex, Cdc42, LIM-kinase, and focal adhesion kinase often coodinately regulate the motility and migration of cancer cell. Although the signaling pathways and molecular mechanisms that regulate cancer cell motility and migration remain to be defined fully,existing data clearly indicate that inhibition of cancer cell motility might be a useful strategy in the management of neoplasm growth and metastasis.