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  • Title: Sodium selenite (Na2SeO3) induces apoptosis through the mitochondrial pathway in CNE-2 nasopharyngeal carcinoma cells.
    Author: Cui Z, Li C, Li X, Zhang Q, Zhang Y, Shao J, Zhou K.
    Journal: Int J Oncol; 2015; 46(6):2506-14. PubMed ID: 25891011.
    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 cytometry 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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