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Originally published In Press as doi:10.1074/jbc.M003965200 on January 29, 2001

J. Biol. Chem., Vol. 276, Issue 18, 14728-14736, May 4, 2001
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Hyaluronic Acid Induces Survival and Proliferation of Human Myeloma Cells through an Interleukin-6-mediated Pathway Involving the Phosphorylation of Retinoblastoma Protein*

Thierry VincentDagger , Michel JourdanDagger , Man-Sun Sy§, Bernard KleinDagger , and Nadir MechtiDagger

From the Dagger  INSERM Unité U475, 99 rue Puech Villa, 34197 Montpellier cedex 5, France and § Institute of Pathology and Cancer Research Center, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106-4943

Originating from a post-switch memory B cell or plasma cell compartment in peripheral lymphoid tissues, malignant myeloma cells accumulate in the bone marrow of patients with multiple myeloma. In this favorable microenvironment their growth and survival are dependent upon both soluble factors and physical cell-to-cell and cell-to-extracellular matrix contacts. In this report we show that hyaluronan (HA), a major nonprotein glycosaminoglycan component of the extracellular matrix in mammalian bone marrow, is a survival and proliferation factor for human myeloma cells. The effect of HA is mainly mediated through a gp 80-interleukin 6 (IL-6) receptor pathway by a CD44-independent mechanism, suggesting that HA retains and concentrates IL-6 close to its site of secretion, thus favoring its autocrine activity. In addition, we show that HA-mediated survival and proliferation of myeloma cells is associated with a down-regulation in the expression of p27kip1 cyclin-dependent kinase inhibitor and a hyperphosphorylation of the retinoblastoma protein (pRb). These data suggest that HA could be an important component in the myeloma cell physiopathology in vivo by potentiating autocrine and/or paracrine IL-6 activities.

* This work was supported by grants from the Association pour la Recherche contre le Cancer, the INSERM, the CNRS, the Federation des Centres de Lutte contre le Cancer Comites de l'Herault et du Gard, the Ligue Contre le Cancer, and the Federation pour la Recherche Medicale.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: INSERM Unité U475, 99 rue Puech Villa, 34197 Montpellier cedex 5, France. Tel.: 4 67 63 62 71; Fax: 4 67 04 18 63; E-mail: mechti@u475.montp.inserm.fr.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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