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Through their heparan sulphate side chains, syndecans may further engage directly in ligand binding 9.I have read and accept the Wiley Online Library Terms and Conditions of Use Shareable Link Use the link below to share a full-text version of this article with your friends and colleagues.
Learn more. Copy URL. ![]() In the brain, the guidance is provided by myelinated axons, astrocyte processes, and blood vessels which are used as invasion routes by glioma cells. In the human breast, containing interstitial collagenrich connective tissue, disseminating breast cancer cells preferentially invade along bundled collagen fibrils and the surface of adipocytes. In both invasion types, physical guidance prompted by interfaces and space is complemented by molecular guidance. Generic mechanisms shared by most, if not all, tissues include (i) guidance by integrins towards fibrillar interstitial collagen andor laminins and type IV collagen in basement membranes decorating vessels and adipocytes, and, likely, CD44 engaging with hyaluronan; (ii) haptotactic guidance by chemokines and growth factors; and likely (iii) physical pushing mechanisms. Tissuespecific, resticted guidance cues include ECM proteins with restricted expression (tenascins, lecticans), cellcell interfaces, and newly secreted matrix molecules decorating ECM fibres (laminin332, thrombospondin1, osteopontin, periostin). We here review physical and molecular guidance mechanisms in interstitial tissue and brain parenchyma and explore shared principles and organspecific differences, and their implications for experimental model design and therapeutic targeting of tumour cell invasion. Copyright 2011 Pathological Society of Great Britain and Ireland. After metastasis to secondary organs, local invasion by cancer cells may lead to secondary organ infiltration, thereby engaging with a tissue environment that differs from the primary organ 1. At any invasion stage, cancer cells are confronted with nonneoplastic tissue composed of cells and cellderived extracellular matrix (ECM). Cancer cells constitutively express adhesion receptors that bind to ECM as well as to resident stromal cells which not only activate the actomyosin machinery to generate traction forces needed to migrate, but also deliver important signals for their growth and survival 2. Initially cancer invasion is largely nondestructive, but over time leads to substantial tissue remodelling, local destruction with ulceration, vessel disruption, and, ultimately, loss of function of invaded organs 3. Both share significant similarities but also show important anatomic and molecular differences that impact upon the invasion process. ![]() Using brain parenchyma and breast stroma as prototypic models for nervous and peripheral connective tissue invasion, respectively, we here review key tissue structures and their molecular properties that enable and guide cancer invasion and discuss the implications for designing experimental models and molecular antiinvasion therapy. References often show trends, with divergent expression regulation in patient subgroups. Eight distinct and 18 chains combine to form 24 different heterodimers with distinct ligand specificity for ECM proteins (eg collagens, laminins, fibronectin, vitronectin, tenascins, thrombospondin, and fibrin) and cell surface receptors (eg ICAM1, VCAM1, and L1CAM) 4, 5. By these means, each cell type maintains a selective and activationdependent integrin repertoire and thus ligand preference. Consequently, integrins are important mediators for cell adhesion and migration. They further contribute to cellcell contacts via direct interactions with counterpart cell receptors or indirectly, by bridging intercellular ECM molecules, including fibronectin or vitronectin 7. Syndecans function mainly as coreceptors by binding to their ECM ligands in conjunction with other receptors, notably integrins 8.
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