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Sodium Selenite Induces Apoptosis in Acute Promyelocytic Leukemia-Derived NB4 Cells Through Mitochondria-Dependent Pathway

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Our previous study has shown that sodium selenite can cause apoptosis in acute promyelocytic leukemia-derived NB4 cells in a caspase-dependent manner involving m disruption and cleavage of Bcl-2, but more detailed mechanism(s) remain unclear. Here we showed that mitochondrial apoptosis signaling pathway played a vital role in apoptosis induced by sodium selenite based on the following findings: 1) cytochrome c release, activation of caspase 9, mitochondrial targeting, and oligermerization of Bax; 2) caspase 9 , but not caspase 8, inhibitor could attenuate apoptosis; 3) downregulation of Bax and Bad by siRNA could delay sodium selenite-induced apoptosis. Further investigation showed that ROS was an essential inducer of m disruption and apoptosis by sodium selenite. Our findings here demonstrate that sodium selenite can induce apoptosis in NB4 cells through a mechanism involving ROS, activation of proapoptotic proteins Bad and Bax, m disruption, release of cytochrome c, and consequent initiation of caspase cascade.
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Keywords: Acute promyelocytic leukemia-derived NB4 cells; Apoptosis; Bcl-2 family; Reactive oxygen species; Sodium selenite

Document Type: Research Article

Publication date: 01 January 2009

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