MK-886 enhances tumour necrosis factor-alpha-induced differentiation and apoptosis
Language English Country Ireland Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
16039040
DOI
10.1016/j.canlet.2005.06.012
PII: S0304-3835(05)00557-4
Knihovny.cz E-resources
- MeSH
- Apoptosis * MeSH
- Arachidonate 5-Lipoxygenase metabolism MeSH
- Cell Differentiation MeSH
- Cell Cycle MeSH
- Time Factors MeSH
- HL-60 Cells MeSH
- Indoles pharmacology MeSH
- Lipoxygenase Inhibitors pharmacology MeSH
- Humans MeSH
- Cell Line, Tumor MeSH
- Signal Transduction MeSH
- Tumor Necrosis Factor-alpha metabolism MeSH
- Cell Survival MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Arachidonate 5-Lipoxygenase MeSH
- Indoles MeSH
- Lipoxygenase Inhibitors MeSH
- MK-886 MeSH Browser
- Tumor Necrosis Factor-alpha 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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