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Monocytic differentiation of leukemic HL-60 cells induced by co-treatment with TNF-alpha and MK886 requires activation of pro-apoptotic machinery
J. Procházková, L. Stixová, K. Souček, J. Hofmanová, A. Kozubík
Jazyk angličtina Země Velká Británie
Typ dokumentu práce podpořená grantem
E-zdroje NLK
Medline Complete (EBSCOhost) od 2000-01-01 do Před 1 rokemWiley Online Library (archiv) od 1997-01-01 do 2012-12-31
- MeSH
- aktivace enzymů účinky léků MeSH
- akutní promyelocytární leukemie farmakoterapie metabolismus patologie MeSH
- apoptóza fyziologie účinky léků MeSH
- buněčná diferenciace účinky léků MeSH
- chloromethylketony aminokyselin farmakologie MeSH
- HL-60 buňky MeSH
- indoly farmakologie MeSH
- inhibitory cysteinových proteinas farmakologie MeSH
- inhibitory lipoxygenas farmakologie MeSH
- kaspasy antagonisté a inhibitory metabolismus MeSH
- lidé MeSH
- MAP kinasový signální systém účinky léků MeSH
- monocyty patologie účinky léků MeSH
- NF-kappa B antagonisté a inhibitory MeSH
- TNF-alfa farmakologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- práce podpořená grantem MeSH
The block of hematopoietic differentiation program in acute myeloid leukemia cells can be overcome by differentiating agent like retinoic acid, but it has several side effects. A study of other differentiation signaling pathways is therefore useful to predict potential targets of anti-leukemic therapy. We demonstrated previously that the co-treatment of HL-60 cells with Tumor necrosis factor-alpha (TNF-alpha) (1 ng/mL) and inhibitor of 5-lipoxygenase MK886 (5 microm) potentiated both monocytic differentiation and apoptosis. In this study, we detected enhanced activation of three main types of mitogen-activated protein kinases (MAPKs) (p38, c-Jun amino-terminal kinase [JNK], extracellular signal-regulated kinase [ERK]), so we assessed their role in differentiation using appropriate pharmacologic inhibitors. The inhibition of pro-apoptotic MAPKs (p38 and JNK) suppressed the effect of MK886 + TNF-alpha co-treatment. On the other hand, down-regulation of pro-survival ERK pathway led to increased differentiation. Those effects were accompanied by increased activation of caspases in cells treated by MK886 + TNF-alpha. Pan-caspase inhibitor ZVAD-fmk significantly decreased both number of apoptotic and differentiated cells. The same effect was observed after inhibition of caspase 9, but not caspase 3 and 8. To conclude, we evidenced that the activation of apoptotic processes and pathways supporting apoptosis (p38 and JNK MAPKs) is required for the monocytic differentiation of HL-60 cells.
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- $a Monocytic differentiation of leukemic HL-60 cells induced by co-treatment with TNF-alpha and MK886 requires activation of pro-apoptotic machinery / $c J. Procházková, L. Stixová, K. Souček, J. Hofmanová, A. Kozubík
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- $a Department of Cytokinetics, Institute of Biophysics, Academy of Sciences of Czech Republic, vvi, Brno, Czech Republic.
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- $a The block of hematopoietic differentiation program in acute myeloid leukemia cells can be overcome by differentiating agent like retinoic acid, but it has several side effects. A study of other differentiation signaling pathways is therefore useful to predict potential targets of anti-leukemic therapy. We demonstrated previously that the co-treatment of HL-60 cells with Tumor necrosis factor-alpha (TNF-alpha) (1 ng/mL) and inhibitor of 5-lipoxygenase MK886 (5 microm) potentiated both monocytic differentiation and apoptosis. In this study, we detected enhanced activation of three main types of mitogen-activated protein kinases (MAPKs) (p38, c-Jun amino-terminal kinase [JNK], extracellular signal-regulated kinase [ERK]), so we assessed their role in differentiation using appropriate pharmacologic inhibitors. The inhibition of pro-apoptotic MAPKs (p38 and JNK) suppressed the effect of MK886 + TNF-alpha co-treatment. On the other hand, down-regulation of pro-survival ERK pathway led to increased differentiation. Those effects were accompanied by increased activation of caspases in cells treated by MK886 + TNF-alpha. Pan-caspase inhibitor ZVAD-fmk significantly decreased both number of apoptotic and differentiated cells. The same effect was observed after inhibition of caspase 9, but not caspase 3 and 8. To conclude, we evidenced that the activation of apoptotic processes and pathways supporting apoptosis (p38 and JNK MAPKs) is required for the monocytic differentiation of HL-60 cells.
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