1,25-Dihydroxyvitamin D3 protects human leukemic cells from tumor necrosis factor-induced apoptosis via inactivation of cytosolic phospholipase A2.
作者： Stephen M. Kelsey , Adrian C. Newland , Xu-Rong Jiang , Paul D. Allen , Yu-Ling Wu
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摘要: Abstract The mechanism by which tumor necrosis factor (TNF) induces death of cancer cells appears to involve the activation cytosolic phospholipase A 2 (cPLA ). U937 human leukemic treated with 1,25-dihydroxyvitamin D 3 [1,25(OH) ; 10 -8 m] become resistant TNF, an effect that is independent cell cycle status and expression TNF receptors or BCL-2. In this study, produced a dose- time-dependent enhancement [ H]arachidonic acid release in cells. amount was positively associated TNF-induced apoptosis. Both immunofluorescence microscopy Western blotting subcompartments demonstrated translocation cPLA from cytosol membrane response TNF. addition, up-regulated mRNA. An antisense oligonucleotide inhibitor 4-bromophenacyl bromide significantly inhibited cytotoxicity. Prior incubation 1,25(OH) ( ) apoptosis, b thermore, inhibitory not reversed inhibitors transcription translation. data suggest involved apoptosis directly inhibits mRNA up-regulation induced Disruption may represent possible whereby can TNF-mediated killing.
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