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Blood, Vol. 94 No. 5 (September 1), 1999:
pp. 1747-1754
Human Immunodeficiency Virus-1 (HIV-1)-Tat Protein Promotes Migration
of Acquired Immunodeficiency Syndrome-Related Lymphoma Cells and
Enhances Their Adhesion to Endothelial Cells
Renato G.S. Chirivi,
Giulia Taraboletti,
Maria Rosa Bani,
Luca Barra,
Giampiero Piccinini,
Mauro Giacca,
Federico Bussolino, and
Raffaella Giavazzi
From Laboratory of the Biology and Treatment of Metastasis and
Laboratory of Cellular and Molecular Biology of the Immune Response and
Auto Immunity, Mario Negri Institute for Pharmacological Research,
Bergamo, Italy; International Centre for Genetic Engineering and
Biotechnology (ICGEB), Trieste, Italy; and Institute for Cancer
Research and Treatment (I.R.C.C.), School of Medicine, University of
Turin, Candiolo, Italy.
Human immunodeficiency virus-1 (HIV-1)-Tat, the transactivating gene
product of HIV-1, has been shown to interact with different cell types,
inducing gene expression, altering their growth and migratory behavior.
In this study we examined whether Tat might affect functions of
acquired immunodeficiency syndrome (AIDS)-related non-Hodgkin's
lymphoma (NHL), relevant to the in vivo dissemination. Our results show
that Tat significantly augmented the motility of the two AIDS-related
Burkitt's lymphoma cell lines (AS283 and PA682PB) and AIDS-primary
effusion lymphoma cell line (HBL-6-AIDS-PEL). Mutations in RGD or basic
domain of Tat (KGE-MBP and LxI-MBP, respectively) sharply reduced
migration compared with wild type, suggesting that both domains are
required for migration. In contrast, a Tat protein
mutation outside the active domains (NH2-TAT-GST) did not
reduce lymphoma cell migration. The treatment of lymphoma cells with
Tat did not influence their adhesion to matrix proteins or to human
vascular endothelial cells, but endothelial cells treated with Tat
became more adhesive to lymphoma cells. Flow cytometric analysis showed
that treatment of endothelial cells with Tat induced the cell surface
expression of the adhesion molecules vascular cell adhesion molecule-1
(VCAM-1) and E-selectin and increased the expression of intercellular
adhesion molecule-1 (ICAM-1). Only antibodies against
VCAM-1 on endothelial cells or against the VLA-4 integrin expressed on
AS283 cells inhibited the increment of adhesion, indicating the
relevance of this pathway in the adhesion of lymphoma cells to vascular
endothelium. In our work, we show for the first time that Tat can
enhance the migration of lymphoma cells and their adhesion to
endothelial cells, two processes that may contribute to the malignant
behavior of NHL in patients with AIDS.
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