Runx2, a runt-related transcriptional factor family member, is involved in the 
regulation of osteoblast differentiation. Interestingly, it is abundant in 
growth-arrested 3T3-L1 preadipocytes and was dramatically down-regulated during 
adipocyte differentiation. Knockdown of Runx2 expression promoted 3T3-L1 
adipocyte differentiation, whereas overexpression inhibited adipocyte 
differentiation and promoted the trans-differentiation of 3T3-L1 preadipocytes 
to bone cells. Runx2 was down-regulated specifically by dexamethasone (DEX). 
Only type I Runx2 was expressed in 3T3-L1 preadipocytes. Using luciferase assay 
and chromatin immunoprecipitation-quantitative PCR analysis, it was found that 
DEX repressed this type of Runx2 at the transcriptional level through direct 
binding of the glucocorticoid receptor (GR) to a GR-binding element in the Runx2 
P2 promoter. Further studies indicated that GR recruited histone deacetylase 1 
to the Runx2 P2 promoter which then mediated the deacetylation of histone H4 and 
down-regulated Runx2 expression. Runx2 might play its repressive role through 
the induction of p27 expression, which blocked 3T3-L1 adipocyte differentiation 
by inhibiting mitotic clonal expansion. Taken together, we identified Runx2 as a 
new downstream target of DEX and explored a new pathway between DEX, Runx2, and 
p27 which contributed to the mechanism of the 3T3-L1 adipocyte differentiation.