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Interleukin-6 and transforming growth-factor-beta synergistically stimulate chondrosarcoma cell-proliferation

Academic Article
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Overview

authors

  • Guerne, P. A.
  • Lotz, Martin

publication date

  • 1991

journal

  • Journal of Cellular Physiology  Journal

abstract

  • This study examines the regulation of Swarm rat chondrosarcoma (SRC) cell proliferation in vitro. In serum-free cultures, SRC cells showed only transient DNA synthesis and this was increased by serum. Transforming growth factor-beta (TGF-beta) was identified as an essential serum component, since the mitogenic effect of sera was related to their TGF-beta content and neutralized by antibody to TGF-beta. Among a large panel of agents tested, TGF-beta was the only factor that stimulated proliferation in serum-free media. The TGF-beta isoforms TGF-beta 1 and TGF-beta 2 induced similar dose-dependent increases with maximal 62.5-fold stimulation at 10 ng/ml. Interleukin-6 (IL-6) was identified as a new factor that stimulated SRC proliferation. IL-6 effects were serum-dependent and their magnitude correlated with the TGF-beta content in different serum preparations. In serum-free cultures where IL-6 by itself had no detectable effect it caused up to 7.6-fold increased proliferation in the presence of small doses of TGF-beta (0.01-0.1 ng/ml). This synergy was unique, since no other factor tested synergized with IL-6 or TGF-beta. In examining potential mechanisms for this synergy it was found that TGF-beta increased IL-6 receptor expression. In summary, these results identify IL-6 as a new and TGF-beta as the most potent growth factor for chondrosarcoma cells and describe novel interactions between these factors in the regulation of cell growth.

subject areas

  • Animals
  • Blood
  • Cell Division
  • Cell Line
  • Chondrosarcoma
  • Culture Media
  • DNA, Neoplasm
  • Drug Synergism
  • Growth Substances
  • Interleukin-6
  • Rats
  • Receptors, Immunologic
  • Receptors, Interleukin-6
  • Transforming Growth Factor beta
  • Tumor Cells, Cultured
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Identity

International Standard Serial Number (ISSN)

  • 0021-9541

Digital Object Identifier (DOI)

  • 10.1002/jcp.1041490115

PubMed ID

  • 1939340
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Additional Document Info

start page

  • 117

end page

  • 124

volume

  • 149

issue

  • 1

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