gms | German Medical Science

66th Annual Meeting of the German Society of Neurosurgery (DGNC)
Friendship Meeting with the Italian Society of Neurosurgery (SINch)

German Society of Neurosurgery (DGNC)

7 - 10 June 2015, Karlsruhe

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Analysis of epithelial-to-mesenchymal transition in paired primary and recurrent glioblastomas

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  • Carolin Kubelt - Klinik für Neurochirurgie, UKSH, Campus Kiel
  • Kirsten Hattermann - Anatomisches Institut, CAU zu Kiel
  • Susanne Sebens - Institut für Experimentelle Medizin, Abteilung Inflammatorische Karzinogenese, UKSH, Campus Kiel
  • Maximilian Mehdorn - Klinik für Neurochirurgie, UKSH, Campus Kiel
  • Janka Held-Feindt - Klinik für Neurochirurgie, UKSH, Campus Kiel

Deutsche Gesellschaft für Neurochirurgie. 66. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC). Karlsruhe, 07.-10.06.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. DocP 044

doi: 10.3205/15dgnc442, urn:nbn:de:0183-15dgnc4425

Published: June 2, 2015

© 2015 Kubelt 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

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Objective: Malignant glioblastomas have a median survival time of less than one year which is mainly due to aggressive relapses after therapeutic treatment. They achieve their progressive character via epithelial-to-mesenchymal transition (EMT); however, comparative surveys on EMT in primary glioblastomas versus relapses are presently not available. Thus, our current study examines the expression profile of different EMT-markers in matched primary and recurrent glioblastomas

Method: We examined the expression profile of different EMT-markers in 17 matched primary and recurrent glioblastomas by qPCR and double-immunofluorescence stainings to identify EMT marker expressing cell types. Additionally, we analyzed the influence of temozolomide on EMT marker expression by qPCR.

Results: In comparison to primary tumours, beta-Catenin (p< 0.05), Snail1 (p< 0.05), Snail2 (p< 0.05), biglycan (p< 0.05) and Twist1 (p< 0.01) were downregulated in relapses whereas L1CAM showed an upregulation (p< 0.05). Desmoplakin, Vimentin, Fibronectin, TGF-beta1 (and its receptors) and Akirin2 seemed to be not regulated. Comparing each individual pair, five different "EMT groups" within our glioblastoma collective were identified according to the regulation of mRNA expression of GFAP, Desmoplakin, Snail1, Snail2, Twist1 and Vimentin. Expressions of different EMT markers in combination with cell specific markers (glial fibrillary acidic protein, CD11b, von Willebrand factor) revealed that EMT markers were expressed in a complex pattern with all three cellular types as possible sources. Additionally, temozolomide was able to induce mRNA expression of nearly all investigated EMT markers to significant levels in T98G glioma cells (p< 0.001; p< 0.01; p< 0.05).

Conclusions: EMT seems to be involved in glioma progression in a complex way and is influenced by commonly-used therapeutic options in glioma therapy.