Influence of LOX/COX inhibitors on cell differentiation induced by all-trans retinoic acid in neuroblastoma cell lines
Jazyk angličtina Země Řecko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
20043138
Knihovny.cz E-zdroje
- MeSH
- apoptóza účinky léků MeSH
- buněčná diferenciace účinky léků MeSH
- buněčný cyklus účinky léků MeSH
- celekoxib MeSH
- inhibitory cyklooxygenasy 2 farmakologie MeSH
- inhibitory lipoxygenas farmakologie MeSH
- kyseliny kávové farmakologie MeSH
- lidé MeSH
- nádorové buněčné linie MeSH
- neuroblastom farmakoterapie enzymologie patologie MeSH
- průtoková cytometrie MeSH
- pyrazoly farmakologie MeSH
- sulfonamidy farmakologie MeSH
- tretinoin farmakologie MeSH
- tvar buňky účinky léků MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- caffeic acid MeSH Prohlížeč
- celekoxib MeSH
- inhibitory cyklooxygenasy 2 MeSH
- inhibitory lipoxygenas MeSH
- kyseliny kávové MeSH
- pyrazoly MeSH
- sulfonamidy MeSH
- tretinoin MeSH
We investigated the possible modulation by LOX/ COX inhibitors of all-trans retinoic acid (ATRA)-induced cell differentiation in two established neuroblastoma cell lines, SH-SY5Y and SK-N-BE(2). Caffeic acid, as an inhibitor of 5-lipoxygenase, and celecoxib, as an inhibitor of cyclooxygenase-2, were chosen for this study. The effects of the combined treatment with ATRA and LOX/COX inhibitors on neuroblastoma cells were studied using cell morphology assessment, detection of differentiation markers by immunoblotting, measurement of proliferation activity, and cell cycle analysis and apoptosis detection by flow cytometry. The results clearly demonstrated the potential of caffeic acid to enhance ATRA-induced cell differentiation, especially in the SK-N-BE(2) cell line, whereas application of celecoxib alone or with ATRA led predominantly to cytotoxic effects in both cell lines. Moreover, the higher sensitivity of the SK-N-BE(2) cell line to combined treatment with ATRA and LOX/COX inhibitors suggests that cancer stem cells are a main target for this therapeutic approach. Nevertheless, further detailed study of the phenomenon of enhanced cell differentiation by expression profiling is needed.
Why Differentiation Therapy Sometimes Fails: Molecular Mechanisms of Resistance to Retinoids