Migration and invasion are intriguing processes with constant formation and disassembly of adhesion. Adhesion occurs at protrusions while disassembly of the focal adhesion complex takes place at the cell rear and at the base of protrusions. Focal adhesion kinase (FAK) is an important regulator of cytoskeleton dynamics involved in adhesion and migration (31). Our results suggest that DS-epi1-downregulated cells have a malfunctioning disassembly of adhesion complexes, and abnormal actin cytoskeleton architecture. The induction of FAK and pFAK could be due to increased spreading of IdoA-deficient cells (32). Altered signals could originiate from a modified ECM, deposite by shRNA-a and –b cells over the time of cultivation. The actual presence of IdoA in CS/DS or CS has been overlooked in many cases, especially when considering cell surface bound PGs. An exception is the part time PG CD44 that has been shown to contain IdoA under certain circumstances (33). CD44 is localized in the focal adhesions of invadopodia (34) and has a functional role in the anchoring of cytoskeleton elements to cell membrane in connection with ECM molecules, and in concentrating metalloproteases.
