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  • Title: Activation of p53 by sodium selenite switched human leukemia NB4 cells from autophagy to apoptosis.
    Author: Li Z, Shi K, Guan L, Jiang Q, Yang Y, Xu C.
    Journal: Oncol Res; 2013; 21(6):325-31. PubMed ID: 25198662.
    Abstract:
    It was revealed by our previous research that sodium selenite repressed autophagy accompanied by the induction of apoptosis in human leukemia NB4 cells. The inhibition of autophagy exerted a facilitative effect on apoptosis. In the present study, we further explored the mechanisms underlying the switch from autophagy to apoptosis and elucidated p53 played a key role. Selenite induced phosphorylation of p53 at the vital site Ser15 via p38MAPK and ERK. Subsequently p53 dissociated with its inhibitory protein mouse double minute 2 (MDM2). Meanwhile, the nucleolar protein B23 transferred from the nucleolus to the nucleoplasm and associated with MDM2, probably stabilizing p53. The active p53 participated in the decrease of autophagic protein Beclin-1 and LC-3, as well as activation of apoptosis-related caspases. Furthermore, in p53 mutant U937 leukemia cells, selenite could not elicit such a switch from autophagy to apoptosis, laying emphasis on the crucial role p53 played in this process.
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