Sodium selenite (Na2SeO3) induces apoptosis through the mitochondrial pathway in CNE-2 nasopharyngeal carcinoma cells

Cui,Zhongyi; Li,Caihong; Li,Xiangyong; Zhang,Qunzhou; Zhang,Yuefei; Shao,Jingjing; Zhou,Keyuan

doi:10.3892/ijo.2015.2968

Sodium selenite (Na2SeO3) induces apoptosis through the mitochondrial pathway in CNE-2 nasopharyngeal carcinoma cells

Authors:
- Zhongyi Cui
- Caihong Li
- Xiangyong Li
- Qunzhou Zhang
- Yuefei Zhang
- Jingjing Shao
- Keyuan Zhou
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Affiliations: Institute of Biochemistry and Molecular Biology, Guangdong Medical College, Zhanjiang, Guangdong, P.R. China, Department of Otolaryngology, The Affiliated Hospital of Guangdong Medical College, Zhanjiang, Guangdong, P.R. China
Published online on: April 17, 2015 https://doi.org/10.3892/ijo.2015.2968
Pages: 2506-2514

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Abstract

This study investigated the effect of sodium selenite (Na2SeO3) on proliferation, cell cycle, apoptosis as well as the underlying mechanism in CNE‑2 nasopharyngeal carcinoma (NPC) cells. The CNE‑2 cell line was treated with different concentrations of Na2SeO3, and the effects of Na2SeO3 on cell viability and proliferation were evaluated using Cell Counting kit‑8 (CCK‑8) assay. Cellular apoptosis and cell cycle were evaluated by flow cytomerty following Annexin V‑FITC/PI double staining and PI single staining respectively; nuclei morphology stained with DAPI and Hoechst 333258 was observed under a fluorescence microscope, while DNA fragmentation was detected by agarose gel electrophoresis. The mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) were analyzed using fluorescent staining assays. Expression of Bcl‑XL, Bax, Bak, and caspase‑3 activation were examined by western blotting. The results showed that Na2SeO3 inhibited proliferation and induced apoptosis of CNE‑2 cells in a dose‑ and time‑dependent manner. Na2SeO3 at low concentrations induced cell cycle arrest at S phase, while high concentrations of Na2SeO3 induced cell cycle arrest at G0/G1 phase. Furthermore, Na2SeO3 increased ROS level and decreased MMP, upregulated caspase‑3 activity and the expression of Bak and Bax but simultaneously downregulated Bcl‑XL. In conclusion, our studies demonstrated that Na2SeO3 had significant anti‑proliferative and apoptosis‑inducing effects via arresting cell cycle and regulating mitochondria‑mediated intrinsic caspase pathway in CNE‑2 NPC cells, suggesting that Na2SeO3 might have therapeutic potentials in the treatment of NPC.

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