Abstract
Purpose: To investigate the effect of tricyclic neovibsanin scaffold (TCNS) on cell viability, colony formation capacity and induction of apoptosis in glioma cells. Methods: 3-(4, 5-Dimethylthiazol-2-yl) 2, 5-diphe¬nyltetrazolium bromide (MTT) assay was used to analyze the effect of TCNS on cell proliferation. Light microscopic examination of giemsa solution stained cells was used to calculate the number of colonies with > 50 cells. Flow cytometry using a flow cytometer, while apoptosis detection kit were used to analyze induction of apoptosis. Results: TCNS treatment significantly inhibited the viability of U138 NS and U138 AC cells in a concentration-dependent manner (p < 0.05). TCNS caused 86 % reduction in the capacity of U138 NS cells to form colonies and led to significant induction of apoptosis. The activation of caspase 3 and expression of Bax was increased significantly (p < 0.05). Moreover, TCNS treatment increased the median survival time of mice bearing glioma to 34 days compared to 22 days in untreated mice. Conclusion: Thus, TCNS treatment significantly inhibits the viability of glioma cells and colony formation, but induces apoptosis and increases the median survival of mice. Hence, TCNS may be of therapeutic value for the treatment of glioma.
Highlights
Glioma is the most frequently detected primary brain tumor in adults and has a median survival time of around 3 months for patients availing no treatment [1]
The present study was performed to investigate the effect of tricyclic neovibsanin scaffold (Figure 1) on cell proliferation, colony formation capacity and induction of apoptosis in glioma cells
The results of MTT assay revealed that tricyclic neovibsanin scaffold (TCNS) treatment inhibited the viability of U138 NS and U138 AC cells in concentration dependent manner
Summary
Glioma is the most frequently detected primary brain tumor in adults and has a median survival time of around 3 months for patients availing no treatment [1]. The present study was performed to investigate the effect of tricyclic neovibsanin scaffold (Figure 1) on cell proliferation, colony formation capacity and induction of apoptosis in glioma cells. After 45 min normal goat serum was applied to block the cell samples followed by overnight incubation with anti-mouse CD133/1 monoclonal and GFAP polyclonal primary antibodies. Fetal bovine serum (FBS) and Dulbecco's modified Eagle's medium (DMEM) were purchased from Life Technologies The cells after treatment with TCNS were harvested using trypsinization and rinsed in phosphate buffered saline twice. Differences were considered significant statistically at p < 0.05
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