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Blood, Vol. 94 No. 6 (September 15), 1999:
pp. 2080-2089
Interleukin-6 Regulation of Matrix Metalloproteinase (MMP-2 and
MMP-9) and Tissue Inhibitor of Metalloproteinase (TIMP-1)
Expression in Malignant Non-Hodgkin's Lymphomas
Anna E. Kossakowska,
Dylan R. Edwards,
Christopher Prusinkiewicz,
Melissa C. Zhang,
Dianlin Guo,
Stefan J. Urbanski,
Thomas Grogan,
Leah A. Marquez, and
Anna Janowska-Wieczorek
From the Department of Pathology, University of Calgary, Calgary
Laboratory Services, Calgary, Alberta, Canada; School of Biological
Science, University of East Anglia, Norwich, Norfolk, UK; Department of
Epidemiology, Prevention and Screening, Alberta Cancer Board, Calgary,
Alberta, Canada; SWOG Lymphoma Lab, Tucson, AZ; Canadian Blood Services
and Department of Medicine, University of Alberta, Edmonton, Alberta,
Canada.
We showed previously that human malignant non-Hodgkin's lymphomas
(NHL) degrade extracellular matrix (ECM) components through the action
of metalloproteinases and that elevated expression of matrix
metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1
(TIMP-1) correlated with a poor clinical outcome in patients with NHL.
In the present study we sought to investigate whether there is any
correlation between the expression of gelatinases (MMP-2 and MMP-9),
TIMP-1, and the expression of cytokines and growth factors such as
interleukin-1 (IL-1), IL-6, IL-10, tumor necrosis factor 
(TNF-), transforming growth factor (TGF), and basic
fibroblast growth factor (bFGF) in human NHL. In lymphoma tissues
obtained from 32 patients, elevated expression of IL-6 correlated
significantly with elevated messenger RNA (mRNA) levels of MMP-9,
MMP-2, and TIMP-1. Moreover, in human lymphoid cell lines of B- and
T-cell origin (Raji, Jurkat, and NC-37), IL-6 stimulated production of
MMP-9 and MMP-2 but not TIMP-1. In the Matrigel invasion assay IL-6
significantly upregulated transmigration of Raji and Jurkat
cells, which in turn was inhibited by recombinant human TIMP-1
and anti-MMP-9 and MMP-2 antibodies. We postulate that IL-6 may
play a role in the clinical aggressiveness of human NHL by
stimulating MMP production.
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