Domains of Laminin and Basement Membrane Collagen which Play a Role in Metastases

Liotta, Lance A.; Rao, N C; Barsky, Sanford H.; Turpeenniemi‐Hujanen, Taina

doi:10.1007/978-1-4613-2635-9_19

Cited by 3 publications

(1 citation statement)

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“…60 ' 65,66,93,94,124 One or more globular end regions of the short arms, in addition to promoting cell spreading and binding to plasma membrane sulfatides, bind to type IV collagen. 56,60,65,66 The type IV collagen-binding site for laminin is located approximately 125 nm from the carboxyl-terminal globular domain. 56 The second step of tumor cell invasion of the extracellular matrix is local degradation of the matrix by tumor cell-associated proteolytic enzymes.…”

Section: Biochemical Steps Involved In Tumor Invasionmentioning

confidence: 99%

Proteolytic Enzymes in Cancer Invasion and Metastasis

Goldfarb¹,

Liotta²

1986

Semin Thromb Hemost

142

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The biochemical and molecular basis of the mechanisms involved in tumor invasion and metastasis is currently under intense study, 40,41,62,83,104,127 since cancer metastasis is the major cause of treatment failure, morbidity, and death for patients with solid malignant tumors. 14,26,27,56,81,90,113 Whereas the treatment modalities of surgery, chemotherapy, and radiotherapy can cure approximately 50% of patients who develop malignant tumors, the majority of patients who fail to respond to these modalities succumb to the direct effect of the metastases or to complications associated with the treatment of metastases. 14 ' 56 At the time of diagnosis of primary tumors, approximately 50% of patients already have subclinically occult micrometastatic tumor colonies that ultimately expand and lead to direct anatomic compromise. A large clinically detectable metastatic focus in a particular organ may indeed indicate the presence of numerous occult micrometastases of more recent initiation. The scattered anatomic deposits of metastases, the heterogeneity of their cellular subpopulations, and their size and age variations often prevent surgical removal and limit the response to systemic anticancer agents. 14,55,56 In addition, whereas conventional therapy, such as chemotherapy or radiotherapy, can in some instances retard metastatic growth, conventional therapy can often indirectly lead to patient morbidity and death by compromising the immune response resulting in complications of infectious disease. 56 It is likely that the exploration of the biochemical and molecular mechanisms involved in cancer invasion and metastasis will reveal insights that will contribute to the improved diagnosis and therapy of established human metastatic disease. 55,56 After a brief summary of the interaction of invasive tumor cells with host extracellular matrices, we will review a three-step hypothesis describing the sequence of biochemical processes that take place during tumor cell invasion of the extracellular matrix: matrix attachment, matrix dissolution, and tumor cell locomotion. 55,56 This review will emphasize the role of a broad array of cell-associated proteolytic enzymes that lead to local degradation of extracellular matrices and their specific components during several phases of cancer invasion and metastasis. In addition, the significance of tumor-associated proteolytic enzymes and matrix degradation to the diagnosis of the metastatic aggressiveness of tumors and to the development of therapeutic strategies to prevent local tumor invasion and to treat established human micrometastatic disease is discussed. INTERACTION OF INVASIVE TUMOR CELLS WITH EXTRACELLULAR MATRICESDuring tumor invasion, malignant cells penetrate a variety of extracellular matrices. 33,[43][44][45]55,56,[59][60][61][62][64][65][66][82][83][84] The extracellular matrix is a dense lattice of collagen and elastin embedded within a ground substance consisting of glycoproteins and proteoglycans. The matrix is a supporting scaffold that mediates cell attachment, del...

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Section: Biochemical Steps Involved In Tumor Invasionmentioning

confidence: 99%