Abstract 1539: Impact of glioma cell gene expression due to semaphorin expression

Malignant brain tumours, like the Glioblastoma multiforme, belong to the most frequent tumours encountered in childhood. Unfortunately, even with optimal therapy, consisting of surgical resection and radiotherapy, a glioblastoma multiforme is essentially incurable. In contrast to the excellent results of well established treatment studies in pediatric patients suffering from leukaemia the cure rates of children with malignant brain tumors remained low. That is why the development of new antitumor strategies has become a major issue in experimental neurology. Class-3 semaphorins were first identified as glycoproteins that negatively mediate neuronal guidance by binding to neuropilin. The discovery of more widespread expression of class-3 semaphorins in different tumour cell types implicates a role in tumour biology. The overexpression of class-3 semaphorins in breast cancer cells leads to inhibition of tumour growth. We overexpressed class-3 semaphorins in the human glioma cell line U87MG and monitored a reduction of tumour growth after intracerebral implantation into mice, too. We were also able to detect changes in adhesion and migration. To determine the variation of tumour cell behaviour we analysed the gene expression profile of class-3 overexpressing cells via microarray analysis. We validated changes in transcription levels with the help of realtime-PCR. Changes in the gene expression levels of cell adhesion molecule 2 and Integrin alpha 7 confirmed the changes in adhesion and migration of class-3 semaphorin expressing glioma cells. Further investigations of changes in gene expression levels of different genes are needed to determine the effect of semaphorins on adhesion and migration and the determine the use of class-3 semaphorins as anti-tumour agent. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1539. doi:10.1158/1538-7445.AM2011-1539