Bis induces growth inhibition and differentiation of HL-60 cells via up-regulation of p27
Experimental & Molecular Medicine
;
: 624-630, 2005.
Article
Dans Anglais
| WPRIM
| ID: wpr-24111
ABSTRACT
Bis (Bag-3, CAIR), a Bcl-2-interacting protein, promotes the anti-apoptotic activity of Bcl-2 and increased levels of Bis have been observed in several disease models. The involvement of Bcl-2 and some Bcl-2-binding proteins in differentiation has recently been reported. However, the relevance of Bis to cellular differentiation remains unknown. The findings herein show that Bis expression is up-regulated during the differentiation of HL-60 cells. To investigate the effect of Bis expression on differentiation, we established Bis-overexpressing HL-60 cells (HL-60-bis). HL-60-bis cells have a low nuclear cytoplasmic ratio and indented nucleus in Wright- Giemsa staining, and an increased expression of CD11b in immunofluorescence study, indicating the promotion of differentiation. The overexpression of Bis also resulted in a retarded cell growth rate, accompanied by the accumulation of HL-60 cells at the G0/G1 phase of the cell cycle, which was sustained during the differentiation process. Western blot analysis revealed that the expression of p27, a representative inducer of cell cycle arrest at the G1 phase, was increased 2.5-fold in HL-60-bis cells compared to HL-60-neo cells. These results suggest that the Bis induced growth inhibition of HL-60 cells promotes G0/G1 phase arrest via up-regulation of p27, which seems to be a prerequisite for differentiation. Further studies will be required to define the exact roles of Bis on cellular differentiation more precisely.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Protéines de transport
/
Expression des gènes
/
Différenciation cellulaire
/
Régulation positive
/
Cellules cultivées
/
Cellules HL-60
/
Prolifération cellulaire
/
Forme de la cellule
/
Inhibiteur p27 de kinase cycline-dépendante
/
Cytométrie en flux
Type d'étude:
Étude pronostique
Limites du sujet:
Humains
langue:
Anglais
Texte intégral:
Experimental & Molecular Medicine
Année:
2005
Type:
Article
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