Nuclear topography and expression of the BCR/ABL fusion gene and its protein level influenced by cell differentiation and RNA interference
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
PubMed
15978941
DOI
10.1016/j.leukres.2005.01.011
PII: S0145-2126(05)00055-X
Knihovny.cz E-zdroje
- MeSH
- antigeny povrchové účinky léků genetika MeSH
- apoptóza účinky léků fyziologie MeSH
- bcr-abl fúzové proteiny genetika MeSH
- buněčná diferenciace účinky léků fyziologie MeSH
- buněčné jádro účinky léků genetika metabolismus MeSH
- buňky K562 MeSH
- chronická myeloidní leukemie genetika metabolismus patologie MeSH
- down regulace MeSH
- HL-60 buňky MeSH
- lidé MeSH
- molekulární sekvence - údaje MeSH
- nádorové buněčné linie MeSH
- regulace genové exprese u leukemie * MeSH
- RNA interference fyziologie MeSH
- tetradekanoylforbolacetát analogy a deriváty farmakologie MeSH
- western blotting MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- antigeny povrchové MeSH
- bcr-abl fúzové proteiny MeSH
- phorbolol myristate acetate MeSH Prohlížeč
- tetradekanoylforbolacetát MeSH
Nuclear topography, expression of the BCR/ABL fusion gene and its protein level/cellular pattern were studied in CML cell line K562 stimulated to differentiation, apoptosis and influenced by ABL-RNA interference (ABL-RNAi). Phorbol ester-induced maturation of K562 cells was accompanied by repositioning of down-regulated BCR/ABL genes closer to the nuclear membrane. This nuclear rearrangement could be connected with differentiation-related heterochromatinization of the amplified BCR-ABL locus, as demonstrated by increased histone H3(K9) dimethylation and decreased H3(K9) acetylation of B3A2 breakpoint. Topography of BCR/ABL in differentiated K562 cells was compared with other leukemic cell types: PMA-maturation of HL60 cells did not influence the nuclear positioning of individual BCR and ABL genes. Moreover, BCR and ABL genes in non-stimulated HL60 as well as in the bone marrow cells of CML patients, i.e. also BCR/ABL fusion genes, were positioned more interiorly in comparison with BCR/ABL multiple loci of K562 cells. Decreased expression of BCR/ABL gene was also found after cell stimulation by selectively pro-apoptotic agent etoposide and by ABL-RNAi leading to apoptosis. In order to compare the efficiency of selected experimental strategies, levels of Bcr/Abl and c-Abl proteins were determined and in all cases tested were reduced. In K562 cells the Bcr/Abl and c-Abl proteins were distributed homogeneously in both the cell nucleus and cytoplasm, while differentiation of K562 cells was characterized by a distinct pattern of Bcr/Abl and c-Abl proteins that were focally distributed rather in the cytoplasm while apoptotic population was completely absent of Bcr/Abl and c-Abl signals.
Citace poskytuje Crossref.org
GENBANK
AJ131466
