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Published on: March 18, 2014
Sodium selenite-induced apoptosis mediated by ROS attack in human osteosarcoma U2OS cells
Xiao-Jia Chen1, Fei-Die Duan, Hui-Hua Zhang
1National Engineering Research Center of Genetic Medicine, Guangdong Provincial Key Laboratory of Bioengineering Medicine, Bioengineering Institute of Jinan University, Guangzhou 510632, China. tchenxj@jnu.edu.cn
Abstract:
Sodium selenite (Na(2)SeO(3), SSE) is an inorganic Se compound that is widely used in cancer chemoprevention studies. SSE has been shown to have anti-proliferative effects on several types of human cancer cells, but its effect on osteosarcoma cells has thus far not been reported. In this study, the cytotoxic effect of SSE on osteosarcoma cells U2OS was investigated in vitro and found to be higher than on comparable non-cancer cell lines 293 and L6. Treatment with SSE decreased cell growth in a dose- and time-dependent manner and altered cellular morphology. SSE also inhibited cell viability by inducing apoptosis, as evidenced by the formation of apoptotic bodies, generation of reactive oxygen species (ROS), and accumulation of cells during the advanced phase of apoptosis. SSE-induced apoptosis correlated with the activation of CASP 3, downregulation of BCL-2, and upregulation of P53 and PTEN in U2OS cells. These results indicated that SSE induces apoptosis in U2OS cells mainly through an ROS-mediated caspase pathway. This is the first report to show a possible mechanism of the anti-proliferative effect of SSE for the prevention of osteosarcoma in cell culture models.
Insights
Sodium selenite (SSE) exhibits potent anti-cancer properties, effectively inhibiting osteosarcoma cell growth and inducing apoptosis. This study reveals SSE
Area of Science:
- Oncology
- Cell Biology
- Biochemistry
Background:
- Sodium selenite (SSE) is an inorganic selenium compound utilized in cancer chemoprevention.
- Previous studies show SSE's anti-proliferative effects on various cancer cells.
- The impact of SSE on osteosarcoma cells remains uninvestigated.
Purpose of the Study:
- To investigate the cytotoxic effects of SSE on human osteosarcoma U2OS cells in vitro.
- To elucidate the mechanism underlying SSE-induced apoptosis in osteosarcoma cells.
Main Methods:
- In vitro cell culture of U2OS osteosarcoma cells and non-cancerous cell lines (293, L6).
- Treatment with varying doses and durations of SSE.
- Assessment of cell viability, proliferation, morphology, apoptosis markers (apoptotic bodies, ROS), and key protein expression (CASP 3, BCL-2, P53, PTEN).
Main Results:
- SSE demonstrated higher cytotoxicity against U2OS cells compared to non-cancer cell lines.
- SSE inhibited cell growth and altered cell morphology in a dose- and time-dependent manner.
- SSE induced apoptosis via ROS generation, CASP 3 activation, BCL-2 downregulation, and P53/PTEN upregulation, indicating a ROS-mediated caspase pathway.
Conclusions:
- Sodium selenite effectively induces apoptosis in osteosarcoma U2OS cells through a ROS-mediated caspase pathway.
- This study provides the first evidence of SSE's anti-proliferative mechanism in osteosarcoma cell models.
- SSE shows potential for osteosarcoma chemoprevention.
