Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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Originally published online as doi:10.1189/jlb.0607397 on March 13, 2008

Published online before print March 13, 2008
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(Journal of Leukocyte Biology. 2008;83:1484-1492.)
© 2008 by Society for Leukocyte Biology

S100A8/A9 at low concentration promotes tumor cell growth via RAGE ligation and MAP kinase-dependent pathway

Saeid Ghavami*,1, Iran Rashedi*,1, Brian M. Dattilo{dagger}, Mehdi Eshraghi*, Walter J. Chazin{dagger}, Mohammad Hashemi{ddagger}, Sebastian Wesselborg§, Claus Kerkhoff||,2 and Marek Los,2,3

* Manitoba Institute of Cell Biology and Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, Manitoba, Canada;
|| Institute of Experimental Dermatology, Münster, Germany;
{dagger} Departments of Biochemistry, Physics and Chemistry, Center for Structural Biology, Vanderbilt University, Nashville, Tennessee, USA;
{ddagger} Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Science, Zahedan, Iran;
§ Department of Internal Medicine I, University of Tübingen, Tübingen, Germany; and
BioApplications Enterprises, Winnipeg, Manitoba, Canada

3Correspondence: BioApplications Enterprises, 34 Vanier Dr., Winnipeg, R2V 2NG, MB, Canada. E-mail: mjelos{at}gmail.com

The complex formed by two members of the S100 calcium-binding protein family, S100A8/A9, exerts apoptosis-inducing activity against various cells, especially tumor cells. Here, we present evidence that S100A8/A9 also has cell growth-promoting activity at low concentrations. Receptor of advanced glycation end product (RAGE) gene silencing and cotreatment with a RAGE-specific blocking antibody revealed that this activity was mediated via RAGE ligation. To investigate the signaling pathways, MAPK phosphorylation and NF-{kappa}B activation were characterized in S100A8/A9-treated cells. S100A8/A9 caused a significant increase in p38 MAPK and p44/42 kinase phosphorylation, and the status of stress-activated protein kinase/JNK phosphorylation remained unchanged. Treatment of cells with S100A8/A9 also enhanced NF-{kappa}B activation. RAGE small interfering RNA pretreatment abrogated the S100A8/A9-induced NF-{kappa}B activation. Our data indicate that S100A8/A9-promoted cell growth occurs through RAGE signaling and activation of NF-{kappa}B.

Key Words: NF-{kappa}B • proliferation • MRP8 • MRP14 • endokines • S100/calgranulins • cytotoxic peptides




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