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67. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Koreanischen Gesellschaft für Neurochirurgie (KNS)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

12. - 15. Juni 2016, Frankfurt am Main

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Expression of active Transforming-growth factor beta in glioblastomas – TGF-beta as a possible therapeutic target

Meeting Abstract

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  • Stephanie Schipmann - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Germany
  • Juliane Schroeteler - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Germany
  • Michael Schwake - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Germany
  • Walter Stummer - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Germany
  • Christian Ewelt - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Germany
  • Eric Suero - Klinik und Poliklinik für Neurochirurgie, Universitätsklinikum Münster, Germany

Deutsche Gesellschaft für Neurochirurgie. 67. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), 1. Joint Meeting mit der Koreanischen Gesellschaft für Neurochirurgie (KNS). Frankfurt am Main, 12.-15.06.2016. Düsseldorf: German Medical Science GMS Publishing House; 2016. DocP 009

doi: 10.3205/16dgnc384, urn:nbn:de:0183-16dgnc3844

Veröffentlicht: 8. Juni 2016

© 2016 Schipmann et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.

Gliederung

Text

Objective: Transforming growth factor-beta (TGF-beta) is a multifunctional regulatory cytokine that has pleiotropic functions, regulating cell differentiation, proliferation, angiogenesis and immune function. Furthermore, a large body of evidence suggests that TGF-beta has profound effects on tumour biology. These partial contrary functions indicate a context-dependent and cell-specific function of the molecule and show that a well regulated and controlled expression of this cytokine is of outmost importance. TGF-beta is secreted as a latent complex and is activated in vivo by certain mechanisms involving proteases. Only the active form is able to bind the TGF-beta receptors and transduce a signal in the cascade. The activation of these latent forms represents a crucial step in the regulation of TGF-beta-activity. The aim of this study is to analyse the expression of the active form of TGF-beta in glioblastomas.

Method: Active TGF-beta in fresh-frozen glioblastoma tissue was determined using the plasminogen activator inhibitor-I promoter luciferase (PAI/L) assay. For the PAI/L assay, a truncated TGF-beta-inducible PAI-1 promoter was fused to a firefly luciferase reporter gene and subsequently transfected into mink lung epithelial cells (MLECs) generating a highly sensitive TGF-beta-responsive cell line. Appropriate cell lines were analysed.

Results: Active TGF-beta was expressed by glioblastomas in high concentrations. Nine glioblastoma samples were analysed. The medium expression of active TGF-beta was 97.1 pg/mm3 ranging from 10.3 to 377.4 pg/mm3. U87 glioblastoma cells had a medium expression of active TGF-beta of 5.4 pg/mm3 and normal astrocytic cells of 3.3 pg/mm3. These data show that the tumour microenvironment plays an important role in the activation of TGF-beta as active TGF-beta is significantly higher expressed in glioblastoma tissue than in appropriate cell lines.

Conclusions: These findings are consistent with current literature and indicate that TGF-beta plays an important role in the generation of a tumour-supporting microenvironment and contributes to glioblastoma development. These data suggest TGF-beta as a possible therapeutic target in the therapy of glioblastomas.