MK-886 enhances tumour necrosis factor-alpha-induced differentiation and apoptosis
Jazyk angličtina Země Irsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
16039040
DOI
10.1016/j.canlet.2005.06.012
PII: S0304-3835(05)00557-4
Knihovny.cz E-zdroje
- MeSH
- apoptóza * MeSH
- arachidonát-5-lipoxygenasa metabolismus MeSH
- buněčná diferenciace MeSH
- buněčný cyklus MeSH
- časové faktory 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
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- arachidonát-5-lipoxygenasa MeSH
- indoly MeSH
- inhibitory lipoxygenas MeSH
- MK-886 MeSH Prohlížeč
- TNF-alfa 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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