Cytoskeletal network in colon cancer: from genes to clinical application

Colorectal cancer arises from well-defined sequential steps characterised by distinct genetic events. Abnormalities in the expression and functional activity of cell adhesion molecules are implicated in the development and progression of the majority of colorectal cancers. Intercellular (e.g. E-cadherin/catenin complex) and cell-matrix (e.g. integrins) adhesion molecules are more than just cementing substances but regulate cell polarity, differentiation, proliferation, migration and invasion. Many of these cellular events are mediated through their intimate association with the actin cytoskeletal network. A dynamic actin cytoskeleton characterises normal epithelial cells and polymerisation and depolymerisation of actin filaments enables cell shape to change during migration and mitosis. In colorectal cancer, cells lose actin cytoskeletal organisation and normal cell adhesion when they become invasive. Future investigations should allow the unravelling of new cytoskeletal network functions in tumour biology and may lead to the development of novel therapeutic strategies based on the manipulation of its associated molecules.