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MK-886 enhances tumour necrosis factor-alpha-induced differentiation and apoptosis
Štika J., Vondráček J., Hofmanová J., Šimek V., Kozubík A.
Jazyk angličtina Země Irsko
NLK
ScienceDirect (archiv)
od 1993-01-01 do 2009-12-31
- MeSH
- apoptóza MeSH
- arachidonát-5-lipoxygenasa metabolismus MeSH
- buněčná diferenciace MeSH
- buněčný cyklus MeSH
- časové faktory MeSH
- financování organizované MeSH
- HL-60 buňky MeSH
- indoly farmakologie MeSH
- inhibitory lipoxygenas farmakologie MeSH
- lidé MeSH
- nádorové buněčné linie MeSH
- signální transdukce MeSH
- TNF-alfa metabolismus MeSH
- viabilita buněk MeSH
- Check Tag
- lidé MeSH
We investigated the role of the 5-lipoxygenase (5-LOX) pathway of arachidonic acid metabolism in tumour necrosis factor-alpha (TNF-alpha)-induced differentiation of human leukemic HL-60 cells using MK-886, an inhibitor of 5-LOX activating protein. MK-886 augmented cell cycle arrest and differentiation induced by TNF-alpha; however, both effects were probably 5-LOX-independent, because a general LOX inhibitor, NDGA, had no effect. Apoptosis was significantly elevated after combined TNF-alpha and MK-886 treatment, which could be partially associated with changes of Mcl-1 protein expression. NF-kappaB signalling or activation of JNKs were not modulated by MK-886. Thus, in addition to apoptosis, MK-886 can enhance TNF-alpha-induced differentiation.
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- $a Department of Comparative Animal Physiology and General Zoology, Faculty of Science, Masaryk University, CZ-611 37 Brno, Czech Republic
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- $a We investigated the role of the 5-lipoxygenase (5-LOX) pathway of arachidonic acid metabolism in tumour necrosis factor-alpha (TNF-alpha)-induced differentiation of human leukemic HL-60 cells using MK-886, an inhibitor of 5-LOX activating protein. MK-886 augmented cell cycle arrest and differentiation induced by TNF-alpha; however, both effects were probably 5-LOX-independent, because a general LOX inhibitor, NDGA, had no effect. Apoptosis was significantly elevated after combined TNF-alpha and MK-886 treatment, which could be partially associated with changes of Mcl-1 protein expression. NF-kappaB signalling or activation of JNKs were not modulated by MK-886. Thus, in addition to apoptosis, MK-886 can enhance TNF-alpha-induced differentiation.
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