Activation of p53 by Sodium Selenite Switched Human Leukemia NB4 Cells From Autophagy to Apoptosis

• DOI: 10.3727/096504014x14024160459087
• Publication Date: 2014-07-23T23:34:32Z
• Authors: Zhushi Li; Kejian Shi; Liying Guan; Qian Jiang; Yang Yang; Caimin Xu
• Keywords: 0301 basic medicine; Leukemia; Nuclear Proteins; Apoptosis; Proto-Oncogene Proteins c-mdm2; 3. Good health; 03 medical and health sciences; Sodium Selenite; Cell Line, Tumor; Mutation; Autophagy; Humans; Phosphorylation; Tumor Suppressor Protein p53; Nucleophosmin; Protein Binding

It was revealed by our previous research that sodium selenite repressed autophagy accompanied the induction of apoptosis in human leukemia NB4 cells. The inhibition exerted a facilitative effect on apoptosis. In present study, we further explored mechanisms underlying switch from to and elucidated p53 played key role. Selenite induced phosphorylation at vital site Ser15 via p38MAPK ERK. Subsequently dissociated with its inhibitory protein mouse double minute 2 (MDM2). Meanwhile, nucleolar B23 transferred nucleolus nucleoplasm associated MDM2, probably stabilizing p53. active participated decrease autophagic Beclin-1 LC-3, as well activation apoptosis-related caspases. Furthermore, mutant U937 cells, could not elicit such apoptosis, laying emphasis crucial role this process.