Interaction of Metastatic and Non-Metastatic Tumor Lines with Aortic Endothelial Cell Monolayer and Their Underlying Basal Lamina
A common and most important route for the dissemination of neoplastic cells within the body involves invasion and penetration of tumor cells into blood vessels and/or lymphatics (1–3). Following penetration of blood vessels, tumor cells are either carried away passively in the blood stream or remain at the site of vessel invasion where they proliferate and continue to shed emboli into the circulation (4). Tumor cells arrested in the capillary beds of different organs must then invade the endothelial cell lining and its underlying basal lamina in order to escape into the extravascular tissue and find a proper microenvironment where they can establish metastasis (1–3). Electron microscopic studies have shown local dissolution of the subendothelial basement membrane at its region of contact with invading tumor cells (5), thereby suggesting an enzymatic mechanism. Of particular significance are recent studies on the degradation of collagen type IV (6,7), fibronectin (8,9), laminin (10), and sulfated proteoglycans (8,9,11) by metastatic tumor cells because these macromolecules are the predominant structural constituents in basement membranes (8,12,13).
KeywordsHeparan Sulfate Vascular Endothelium Basal Lamina Extra Cellular Matrix Metastatic Tumor Cell
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- 4.Warren, B.A., Chauvin, W.J. and Phillips, J. Blood-borne tumor emboli and their adherence to vessel walls. In: Cancer invasion metastasis: Biologic Mechanisms and Therapy. S.B. Day, et al. (eds). pp. 185–197, New York, Raven Press (1977).Google Scholar
- 8.Kramer, R.H., Vogel, K.G. and Nicolson, G.L. Solubilization and degradation of subendothelial matrix glycoproteins and proteoglycans by metastatic tumor cells. J.Biol.Chem Z57, 2678–2686 (1982).Google Scholar
- 9.Vlodavsky, I., Fuks, Z., Ariav, Y., Altevogt, P. and Schirrmacher, V. Lymphoma cell mediated degradation of sulfated proteoglycans and fibronectin in the subendothelial extracellular matrix: Relationship to tumor cell metastasis. Submitted for publication.Google Scholar
- 10.Liotta, L.A., Goldfarb, R.H., Brundage, R., Siegal, G.P. and Garbisa, S. Effect of plasminogen activator (urokinase), plasmin, and thrombin on glycoprotein and collagenous components of basement membrane.Google Scholar
- 11.Vlodavsky, I., Ariav, Y., Atzmon, R. and Fuks, Z. Tumor cell attach ment to the vascular endothelium and subsequent degradation of the subendothelial extracellular matrix. Exptl.Cell.Res. (1982) in press.Google Scholar
- 18.Dzarlieva, R., Schirrmacher, V. and Fusenig, N. Cytogenetic changes during tumor progression towards invasion, metastasis and immune escape in the Eb/ESb model system. Int.J.Cancer (1982) in press.Google Scholar
- 19.Schirrmacher, V., Cheingsong-Popov, R. and Arnheiter, H. Hepatocyte- tumor cell interaction in vitro. I. Conditions for rosette formation and inhibition by anti H-2 antibody. J.Exp.Med. 211/ 984–989 (1980).Google Scholar
- 20.Lohmann-Matthes, M.-L., Schleich, A., Shantz, G. and Schirrmacher, V. Tumor metastases and cell-mediated immunity in a model system in DBA/2 mice. VII. Interaction of metastasizing and nonmetastasizing tumors with normal tissue in vitro. J.Natl.Cancer Inst 614, 1413–1425 (1980).Google Scholar
- 24.Vlodavsky, I., Ariav, Y., Fuks, Z. and Schirrmacher, V. Lymphoma cell interaction with cultured vascular endothelial cells and with subendothelial basal lamina: attachment, invasion and morphological appearance. Submitted for publication.Google Scholar
- 26.Nakadjima, M., Inmura, T., Diferrante, D.T., Diferrante, N. and Nicolson, G.L. Rates of heparan sulfate degradation correlate with invasive and metastatic activities of B16 melanoma sublines. J.Cell.Biol 91, 119a (1981).Google Scholar