In vitro effects of selenium on human glioblastoma multiforme cell lines

The incidence of brain tumors ranges from 3 to 5 per 100.000 in humans. 2.7% of cancer-related deaths are caused by brain tumors. Primary brain tumors constitute about 2% of malignant diseases. Glioblastoma multiforme (GBM) is caused by the central nervous system-derived glial cells and is the most common (50-60%) form of primary brain tumor. In elderly (45-70), GBM has higher possibility to emerge and has a high invasive phenotype showing a very rapid progression. The aim of this study was to investigate in vitro effects of selenium on human glioblastoma multiforme cells.In the present study, GMS-10 and DBTRG-05MG human glioblastoma multiforme cell lines were used as a model to examine, in the selenomethionine treated and non-treated groups; selenium entering in the cell, proliferation, cytotoxicity, and Ki-67 protein expression. The organic source of selenium, selenomethionine stimulated effects on cell proliferation and cytotoxicity, as these were assessed with WST-1 and lactate dehydrogenase (LDH) tests, respectively. Ki-67 protein expression was determined by western blot and selenium measurements were performed in supernatants and lyzates by using GFAAS.This is the first study to examine SeMet effects on cell growth and death in GMS-10 and DBTRG-05MG cells. According to the results of our research, cells respond to seleno-L-methionine in a dose-dependent and time-dependent manner for both cell lines. As a result of WST-1 test cell proliferation increased at 50 and 100 µM doses, which were considered as low doses by us. With the analyzis of the AAS results, SeMet levels of the cells were determined to be in accordance with viability and cytotoxicity tests.In this study, SeMet, in the in vitro environmental conditions, has decreased proliferation and has shown cytotoxicity in a dose and incubation period dependent manner in both DBTRG-05MG and GMS-10 cells and these parameters are correlated in a large extent with the levels of SeMet entering the cells.In the view of the data obtained from this investigation and the previous data, our results must be supported by new experiments such as apoptosis assays and ELISA methods. This study will yield further studies focusing on the possibility of using SeMet against some types of GBM.