Suberoylanilide hydroxamic acid (SAHA) at subtoxic concentrations increases the adhesivity of human leukemic cells to fibronectin
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
19911379
DOI
10.1002/jcb.22397
Knihovny.cz E-zdroje
- MeSH
- antigeny CD29 metabolismus MeSH
- antitumorózní látky farmakologie MeSH
- apoptóza účinky léků MeSH
- buněčná adheze účinky léků MeSH
- fibronektiny metabolismus MeSH
- kyseliny hydroxamové farmakologie MeSH
- leukemie metabolismus MeSH
- lidé MeSH
- lymfocyty účinky léků metabolismus MeSH
- nádorové buněčné linie MeSH
- paxilin metabolismus MeSH
- polymerázová řetězová reakce s reverzní transkripcí MeSH
- průtoková cytometrie MeSH
- separace buněk MeSH
- vorinostat MeSH
- western blotting MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antigeny CD29 MeSH
- antitumorózní látky MeSH
- fibronektiny MeSH
- kyseliny hydroxamové MeSH
- paxilin MeSH
- vorinostat MeSH
Suberoylanilide hydroxamic acid (SAHA) is an inhibitor of histone deacetylases (HDACs) which is being introduced into clinic for the treatment of hematological diseases. We studied the effect of this compound on six human hematopoietic cell lines (JURL-MK1, K562, CML-T1, Karpas-299, HL-60, and ML-2) as well as on normal human lymphocytes and on leukemic primary cells. SAHA induced dose-dependent and cell type-dependent cell death which displayed apoptotic features (caspase-3 activation and apoptotic DNA fragmentation) in most cell types including the normal lymphocytes. At subtoxic concentrations (0.5-1 microM), SAHA increased the cell adhesivity to fibronectin (FN) in all leukemia/lymphoma-derived cell lines but not in normal lymphocytes. This increase was accompanied by an enhanced expression of integrin beta1 and paxillin, an essential constituent of focal adhesion complexes, both at the protein and mRNA level. On the other hand, the inhibition of ROCK protein, an important regulator of cytoskeleton structure, had no consistent effect on SAHA-induced increase in the cell adhesivity. The promotion of cell adhesivity to FN seems to be specific for SAHA as we observed no such effects with other HDAC inhibitors (trichostatin A and sodium butyrate).
Citace poskytuje Crossref.org
Group I p21-activated kinases in leukemia cell adhesion to fibronectin
Adhesion structures in leukemia cells and their regulation by Src family kinases
