gms | German Medical Science

73. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Griechischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

29.05. - 01.06.2022, Köln

Article

Send article

Licochalcone A – an ADAM9 inhibitor for vestibular schwannoma therapy

Licochalcone A – ein ADAM9 Inhibitor zur Behandlung des Vestibularisschwannoms

Meeting Abstract

Search Medline for

  • Katharina Flock - Universitätsklinikum Würzburg, Klinik und Poliklinik für Neurochirurgie, Würzburg, Deutschland
  • Cordula Matthies - Universitätsklinikum Würzburg, Klinik und Poliklinik für Neurochirurgie, Würzburg, Deutschland
  • Ralf-Ingo Ernestus - Universitätsklinikum Würzburg, Klinik und Poliklinik für Neurochirurgie, Würzburg, Deutschland
  • Mario Löhr - Universitätsklinikum Würzburg, Klinik und Poliklinik für Neurochirurgie, Würzburg, Deutschland
  • Carsten Hagemann - Universitätsklinikum Würzburg, Klinik und Poliklinik für Neurochirurgie, Würzburg, Deutschland
  • presenting/speaker Maria Breun - Universitätsklinikum Würzburg, Pathologie, Würzburg, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 73. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Griechischen Gesellschaft für Neurochirurgie. Köln, 29.05.-01.06.2022. Düsseldorf: German Medical Science GMS Publishing House; 2022. DocV139

doi: 10.3205/22dgnc138, urn:nbn:de:0183-22dgnc1381

Published: May 25, 2022

© 2022 Flock et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

Text

Objective: Recently, we described a disintegrin and metalloproteinase 9 (ADAM9) overexpression by Schwann cells of vestibular schwannoma (VS) and suggested that it might be a marker for VS tumor growth and invasiveness. Consequently, we analyzed the effect of Licochalcone A (LicA), an ADAM9 inhibitor, in VS primary cell cultures regarding its effect on the cells’ viability, migration, ADAM9 expression and cell number.

Methods: Each experiment was performed with at least three different primary VS cell cultures overexpressing ADAM9 as shown by Western-blot analysis. The cells were treated with 20 µM LicA for 2-6 days and metabolic activity evaluated by MTT-assays, migration by xCELLigence as well as alterations of ADAM9 expression by Western-blotting. To assess cell viability, cells were counted in five fields of view utilizing ImageJ.

Results: ADAM9 expression was stable after 6 days LicA treatment. Migration was not inhibited by LicA and there was no inhibition of metabolic activity after 2, 4 or 6 days LicA treatment. In contrast, VS cell numbers decreased significantly after 4 days LicA treatment in 1 of 4 primary VS cell cultures and after 6 days in the other 3 cultures (p=0.008). This effect was masked in the MTT-assay by proliferation of fibroblasts.

Conclusion: Since LicA seems to inhibit VS cell proliferation, it could be a potential chemotherapeutic treatment option to tackle VS.