Sodium selenite induces apoptosis by ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction in human acute promyelocytic leukemia NB4 cells |
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| Authors: | Liying Guan Binshe Han Zhushi Li Fangyuan Hua Fang Huang Wei Wei Yang Yang Caimin Xu |
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| Affiliation: | (1) National Laboratory of Medical Molecular Biology, Institute of Basic Medicine Sciences, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China;(2) Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China |
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| Abstract: | Introduction In this study, we delineated the apoptotic signaling pathways activated by sodium selenite in NB4 cells. Materials and methods NB4 cells were treated with 20 μM sodium selenite for different times. The activation of caspases and ER stress markers, ROS levels, mitochondrial membrane potential and cell apoptosis induced by sodium selenite were analyzed by immunoblotting analysis, DCF fluorescence and flow cytometric respectively. siRNA was used to detect the effect of GADD153 on selenite-induced cell apoptosis. Conclusions Sodium selenite-induced reactive oxygen species generation is an early event that triggers endoplasmic reticulum stress mitochondrial apoptotic pathways in NB4 cells. |
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| Keywords: | Sodium selenite Apoptosis ER stress GADD153 ROS |
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