In Vitroeffects of Selenium on Human Glioblastoma Multiforme Cell Lines: A Preliminary Study

Abstract

SUMMARY -Glioblastoma multiforme (GBM) is caused by the central nervous system-derived glial cells, and represents the most common (50%-60%) form of primary brain tumors. Th e aim of this study was to investigate the in vitro eff ects of selenium on human GBM cells. In the present study, GMS-10 and DBTRG-05MG human GBM cell lines were used as a model to examine selenium entering the cell, cell proliferation, cytotoxicity, DNA fragmentation and Ki-67 protein expression in selenomethionine treated and non-treated groups. Seleno-L-methionine (SeMet) as the organic source of selenium exerted eff ects on cell proliferation and cytotoxicity, as assessed with WST-1 and lactate dehydrogenase (LDH) tests, respectively. Apoptosis was assessed by DNA fragmentation with an enzyme-linked immunosorbent assay. Ki-67 protein expression was determined by Western blotting, while selenium measurements were performed in the supernatants and lysates by using Graphite Furnace Atomic Absorption Spectrometry. Th is is the fi rst study to examine the eff ects of SeMet on cell proliferation and death in GMS-10 and DBTRG-05MG cells. Both GBM cell lines responded to SeMet in a dose-and time-dependent manner. WST-1 test showed that low-dose SeMet treatment (50 and 100 μM) increased cell proliferation. Analysis of intracellular SeMet levels by using AAS showed results consistent with viability and cytotoxicity tests. SeMet treatment for 72 h caused increased DNA fragmentation in both cell lines. In conclusion, our results suggest that SeMet induces cell death at high doses, while increasing cell proliferation at low doses. In the view of the data obtained in this investigation, further studies focusing on the possibility of using SeMet against different types of GBM and in combination with prospect synergic compounds are considered to be worthwhile.

Prognostic Role of Cd44 Expression and Neovascularization Determined by Endoglin (Cd105) in Glioblastoma Patients

“…The potential influence of CD44 on tumor growth and expansion could be exerted in many ways. CD44 probably stimulates proliferation, motility and/or invasiveness of tumor cells (it probably recruites and activates matrix metalloproteinases attached to cell surface) 1,2,18 . It is also possible that CD44 promotes tumor angiogenesis by regulating endothelial cells and/or recruiting, i.e.…”

Therapeutic Potential of Selenium in Glioblastoma

“…Interestingly, Naziroglu's group reported that Se-species stimulate glioblastoma cell death by increasing the mitochondrial ROS generation and the intracellular free calcium concentration through enhanced TRPM2 activation (Ertilav et al, 2019). Nonetheless, protective effects were observed in non-malignant cells such as neurons or microglia cells (Ataizi et al, 2019;Ertilav et al, 2019;Akyuva et al, 2021), suggesting a cellular specificity and higher affinity of Se-species on apoptosis and oxidative stress to glioma cells (Yakubov et al, 2014;Hazane-Puch et al, 2016;Harmanci et al, 2017;Yakubov, 2019). It has been previously reported that low doses of organic and inorganic forms of Se-species have antioxidant properties in malignant cell lines, but there are apoptotic effects with high dose applications (Uguz et al, 2009;Harmanci et al, 2017).…”

Selenium Compounds as Novel Potential Anticancer Agents

“…In the course of the studies, it was found that methylselenol metabolites exhibit multiple beneficial chemopreventive as well as anticancer effects, whereas an excess of hydrogen selenide metabolites in a cell may cause singlestrand DNA breaks (SSBs) [7]. For this reason, it is thought that organic Se compounds are less toxic than inorganic forms that contain Se [6,9]. The anticancer mechanism of Se-containing compounds is mainly based on inducing apoptosis in cells [10], but apart from that, these compounds also affect gene expression and various cell signal pathways, DNA repair/damage, as well as the angiogenesis process or metastasis [11].…”