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Adhesion molecules in lymphoma metastasis.

¹Division of Cell Biology, The Netherlands Cancer Institute, Amsterdam.

Cancer Metastasis Reviews

|May 1, 1991

Summary

Cellular adhesion molecules (CAMs) mediate lymphoid cell metastasis. T-cell hybridomas reveal LFA-1 is crucial for metastasis, while CD31 and CD44 are also key players in lymphoid spread.

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Area of Science:

Immunology
Cell Biology
Cancer Metastasis

Background:

Cellular adhesion molecules (CAMs) on lymphoid cells mediate interactions with other cells and the extracellular matrix.
These CAMs are implicated in the metastatic process of lymphoma cells, with correlations observed between specific CAM expression and metastasis patterns.

Purpose of the Study:

To investigate the mechanisms of widespread lymphoid metastasis using a T-cell hybridoma model.
To identify specific CAMs involved in the invasiveness and metastatic potential of lymphoid cells.

Main Methods:

Utilized T-cell hybridomas to generate panels of highly invasive and non-invasive cell lines.
Assessed invasiveness in hepatocyte and fibroblast monolayers, correlating it with experimental metastasis.
Analyzed the expression of various lymphoid CAMs in relation to metastatic capability.

Main Results:

LFA-1 (lymphocyte function-associated antigen 1) is essential for efficient T-cell hybridoma metastasis, with high expression levels required.
ICAM-2 (intercellular adhesion molecule 2) is suggested as the likely counterstructure for LFA-1.
CD31 (platelet-endothelial cell adhesion molecule 1) and CD44 are identified as primary candidates involved in T-cell hybridoma metastatic spread.

Conclusions:

LFA-1 plays a critical role in lymphoid metastasis, likely interacting with ICAM-2.
CD31 and CD44 are also significant contributors to the metastatic process in T-cell hybridomas.
Certain CAMs, including ICAM-1, VLA-4, MEL-14, and LPAM-1, are not indispensable for metastasis in this model.

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