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JNCI Journal of the National Cancer Institute 1993 85(3):235-240; doi:10.1093/jnci/85.3.235
© 1993 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 85, No. 3, 235-240, February 3, 1993
© 1993 Oxford University Press

Enhancement of Metastatic Potential of Murine and Human Melanoma Cells by Laminin Receptor Peptide G: Attachment of Cancer Cells to Subendothelial Matrix as a Pathway for Hematogenous Metastasis

Giulia Taraboletti, Dorina Belotti, Raffaella Giavazzi, Mark E. Sobel, Vincent Castronovo

Istituto di Ricerche Farmacologiche Mario Negri Bergamo, Italy
Laboratory of Pathology, Division of Cancer Biology, Diagnosis, and Centers, National Cancer Institute Bethesda, Md.

Correspondence to: Giulia Taraboletti, Ph.D., Istituto Mario Negri, via Gavazzeni, 11, 2400 Bergamo, Italy.

Background: Stable anchorage of circulating cancer cells to the vasculature is a critical step in the formation of hematogenous metastases. Although the basement membrane glycoprotein laminin clearly plays a crucial role in this event, the exact interactive pathways among cancer cells, laminin, and the vessel wall have not been elucidated. In a previous study, we identified synthetic peptide G, which contains the laminin-binding domain of the 67-kd laminin receptor and which inhibits tumor cell adhesion to endothelial cells. Purpose: To assess the role of the interaction between laminin and the 67-kd laminin receptor in hematogenous metastasis formation, we studied the effect of peptide G on melanoma cell behavior in vivo and in vitro. Methods: The effect of peptide G and control peptides was studied in vivo on lung retention and colonizing potential of murine (B16BL6) and human (A2058) melanoma cells injected intravenously in C57BL/6 and nude mice, respectively. In addition, their effect on cell adhesion and chemotaxis to laminin and on binding of iodine 125-labeled laminin to cells was studied in vitro. Results: In vivo, pretreatment of cells with peptide G resulted in a two- to 10-fold significant increase in the number of experimental lung metastases. A significant relative increase in lung retention of peptide G-treated tumor cells was observed 48 hours after injection, although after 4 hours a partial reduction was observed. In vitro, peptide G significantly increased laminin binding and cancer cell adhesion to laminin and subendothelial matrix, whereas chemotaxis to laminin was significantly inhibited. Conclusions: Peptide G differentially affected the biological response of cancer cells to laminin. In vitro, it increased laminin binding and cell adhesion to laminin and subendothelial matrix, whereas it inhibited cell chemotaxis to laminin. In vivo, the overall effect of peptide G was an augmentation of lung metastasis. Implications: Our findings suggest that direct adhesion of tumor cells to the subendothelial matrix is a main pathway for hematogenous metastases and that tumor cell-matrix interaction may be more relevant than tumor cell-endothelial cell attachment in this process. [J Natl Cancer Inst 85: 235–240, 1993]


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