Abstract
In recent years the concept of plasticity between invasion modes used by individual cancer cells has been gaining increasing interest in the field. Individually invading tumour cells can be divided into those that use a mesenchymal invasion mode, those that use "amoeboid" invasion and those that can switch between the two modes. The morphological distinctions between these different modes of invasion suggest that the actin cytoskeleton is likely to be a major contributor to the plasticity of cancer cell invasion mechanisms. We have recently investigated this idea by manipulating expression of Tm5NM1, one isoform of the tropomyosin family of actin-associating proteins. In a novel finding, we discovered that stabilizing the actin cytoskeleton via elevated expression of Tm5NM1 specifically inhibits mesenchymal-type cancer cell invasion, without causing transition to "amoeboid" motility-thus stopping the invading cancer cells in their tracks. The present perspective discusses our recent data in the context of current understanding of invasion plasticity and considers how stabilizing actin filaments may inhibit the mesenchymal invasion mode.