Interaction of tumor cells with the extracellular matrix.
Cancer cell invasion of the normal tissue surrounding a growing neoplasm and the subsequent spread (metastasis) of malignant cells throughout the body is the major cause of the morbidity and mortality associated with malignant disease. At the primary tumor site, local invasion may be minimal as in the case of human malignant melanomas. Yet this tumor has the propensity to disseminate widely. On the other extreme, squamous carcinomas of the head and neck may produce a tremendous amount of host tissue destruction at the primary site. These tumors tend to be highly-invasive locally but disseminate more slowly than other forms of cancer such as malignant melanomas. In a like fashion, malignant melanomas tend to be surrounded by only minimal stroma while other tumor types produce a large amount of extracellular matrix themselves or induce matrix production by normal host tissue cells. In spite of the many tumor type specific differences which exist, recent studies in the field of cancer metastasis have identified features that are common to all invasive and metastatic tumors. This includes adhesion of invading tumor cells to host extracellular matrix structures, degradation of host tissue and active tumor cell movement through the partially degraded tissue. The critical events that occur during the invassion and metastatic processes are mediated through interactions between invading tumor cells and the extracellular matrix of the host. The expression of cell surface receptors for extracellular matrix molecules and the synthesis/expression of extracellular matrix molecules, themselves, on the surface of malignant tumor cells are thought to underline the events that are critical to the invasion and metastatic process.
D000818:Animals; D018955:CD36 Antigens; D002401:Cathepsin B / Q000378:metabolism; D002448:Cell Adhesion; D002465:Cell Movement; D005109:Extracellular Matrix; D005353:Fibronectins / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology; D007797:Laminin / Q000378:metabolism; D008264:Macrophages / Q000502:physiology; D003012:Microbial Collagenase / Q000378:metabolism; D009000:Monocytes / Q000502:physiology; D009361:Neoplasm Invasiveness / Q000503:physiopathology; D009362:Neoplasm Metastasis / Q000503:physiopathology; D009363:Neoplasm Proteins / Q000378:metabolism; D009369:Neoplasms / Q000503:physiopathology*; D009374:Neoplasms, Experimental / Q000503:physiopathology; D010960:Plasminogen Activators / Q000378:metabolism; D010973:Platelet Adhesiveness; D011509:Proteoglycans / Q000378:metabolism; D017469:Receptors, Fibronectin; D011971:Receptors, Immunologic / Q000378:metabolism; D017474:Receptors, Laminin; D011975:Receptors, Mitogen / Q000378:metabolism; D019699:Thrombospondins
D018955:CD36 Antigens; D005353:Fibronectins; D006023:Glycoproteins; D007797:Laminin; D009363:Neoplasm Proteins; D011509:Proteoglycans; D017469:Receptors, Fibronectin; D011971:Receptors, Immunologic; D017474:Receptors, Laminin; D011975:Receptors, Mitogen; D019699:Thrombospondins; D010960:Plasminogen Activators; D002401:Cathepsin B; D003012:Microbial Collagenase