Journal
BMB REPORTS
Volume 45, Issue 3, Pages 194-199Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
DOI: 10.5483/BMBRep.2012.45.3.194
Keywords
Autophagy; DAPK; HL60; PP2A; Sodium selenite
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Funding
- National Natural Sciences Foundation of China [31170788, 30970655]
- National Natural Science Foundation of China [31101018]
- Natural Science Foundation of Being [5082015]
- State Key Laboratory [2060204]
- Ministry of Education, China [20091106110025]
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Autophagy has been suggested as a possible mechanism for non-apoptotic death despite evidence from many species that autophagy represents a survival strategy of cells under stress. From our previous findings that supranutritional doses of sodium selenite induced apoptosis in human leukemia cells, now we show autophagic cell death occurred after selenite exposure in HL60, suggested an alternative mechanism for the potential therapeutic properties of selenite. Additionally, Death-associated Protein Kinase (DAPK) performed a significantly increased expression during this process, concomitantly with gradually decreased phosphorylation at Ser(308). We further reveal that the up-regulation of DAPK which depends on selenite-activated ERK had no effect on autophagy. However, activation of DAPK via PP2A-mediated dephosphorylation at Ser(308) serves as a new strategy for autophagy induction. In conclusion, these results indicate that PP2A-mediated activated DAPK sensitizes HL60 cells to selenite, ultimately triggers autophagic cell death pathway to commit cell demise. [BMB reports 2012; 45(3): 194-199]
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