© 1998 by Oxford University Press
Journal Of The National Cancer Institute, Vol 90, 118-123, Copyright © 1998 by Oxford University Press
JE Lehr and KJ Pienta
BACKGROUND: In virtually all patients with advanced prostate cancer, the
disease metastasizes to bone and causes osteoblastic growth. However, the
mechanisms that contribute to bone metastasis are poorly understood. It has
been hypothesized that the bone provides a favorable growth environment for
prostate cancer cells, which nonselectively seed the bone marrow from the
bloodstream. Alternatively, prostate cancer cells may preferentially bind
to bone marrow endothelial cells. We developed an in vitro model of bone
endothelium and tested the hypothesis that prostate cancer cells adhere
preferentially to bone marrow endothelial cells. METHODS: We isolated and
characterized a human bone marrow endothelial (HBME-1) cell line. Cells
were transfected with the simian virus 40 large T antigen for
immortalization. Cell surface receptors were characterized by
immunohistochemistry and flow cytometry. The adhesion of cancer cells to
HBME-1 and to endothelial cell lines from other organs was tested in an in
vitro binding assay as were inhibitors of adhesion. RESULTS: The
immortalized HBME-1 cell line demonstrated many properties characteristic
of endothelial cells, including positive staining for von Willibrand factor
and rapid formation of tubule structures when exposed to extracellular
matrices. In an in vitro assay, prostate cancer cells adhered
preferentially to human bone marrow endothelium when compared with
endothelium derived from other sources. Preferential adhesion was blocked,
in part, by antibodies to galectin-3 and LFA-1. IMPLICATIONS: These data
suggest that the propensity of prostate cancer cells to establish
themselves in bone is due, at least in part, to their preferential adhesion
to human bone marrow endothelial cells.
ARTICLES
Preferential adhesion of prostate cancer cells to a human bone marrow endothelial cell line
University of Michigan Comprehensive Cancer Center, Department of Internal Medicine, Ann Arbor 48109-0946, USA.
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