Sodium butyrate-induced upregulation of p18( INK4C ) gene affects K562 cell G (0)/G (1) arrest and differentiation.
Mol Cell Biochem
; 319(1-2): 9-15, 2008 Dec.
Article
in En
| MEDLINE
| ID: mdl-18642058
ABSTRACT
Histone deacetylase inhibitor sodium butyrate (NaBu) can induce G(0)/G(1) arrest and erythroid differentiation in K562 cells, but the molecular mechanisms underlying this process are unclear. Here we show that both p18( INK4C ) mRNA and protein levels were upregulated during K562 cell erythroid differentiation induced by NaBu. Moreover, the NaBu activation of p18( INK4C ) was dependent on the integrity of Sp1 clusters in the promoter. NaBu caused hyperacetylation of histones H3 and H4 on endogenous p18( INK4C ) promoter and enhanced binding of transcription factor Sp1 in vivo. Also, overexpression of p18( INK4C ) in K562 cells resulted in G(0)/G(1) arrest and partial erythroid differentiation. Our results suggested that NaBu-mediated p18( INK4C ) regulation played a role in cell cycle arrest and erythroid differentiation in K562 cells.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Butyrates
/
Cell Differentiation
/
Up-Regulation
/
Resting Phase, Cell Cycle
/
G1 Phase
/
Cyclin-Dependent Kinase Inhibitor p18
Limits:
Humans
Language:
En
Journal:
Mol Cell Biochem
Year:
2008
Type:
Article
Affiliation country:
China