Nucleic Acids Research, Vol 24, Issue 14 2849-2856, Copyright © 1996 by Oxford University Press
LF Doerksen, A Bhattacharya, P Kannan, D Pratt and MA Tainsky
HOX A genes are induced in a temporal fashion after retinoic acid (RA)
treatment in non-N-ras-transformed PA-1 human teratcarcinoma cells.
However, In N-ras-transformed PA-1 cells, RA-Induced expression of HOX A
genes is delayed. The mRNA for the transcriptional activator AP-2 is
overexpressed in these ras-transformed cells, but AP-2 transcriptional
activity is inhibited relative to non ras-transformed PA-1 cells.
Constitutive expression of AP-2 mimics the effect of ras by transforming
cells and inhibiting differentiation in culture. We analyzed 4 kb of the
human HOX A4 gene promoter and identified seven putative AP-2-binding sites
in the DNA sequence. Transcription assays with variably sized HOX A4
promoter reporter constructs revealed that a 365 bp region of the promoter,
-2950 to -3315 relative to the mRNA start, controls RA responsiveness and
ras-mediated inhibition of HOX A4 activity. This region contains an AP-2
binding site and a RARE. Elimination of the AP-2 site by site-directed
mutagenesis demonstrated that the AP-2 site is involved in RA-mediated
transcriptional activation of the human HOX A4 promoter in combination with
the RA receptor response element (RARE). In N-ras-transformed cells, low
HOX A4 promoter activity results from ras inhibition of AP-2
transactivation.
ARTICLES
Functional interaction between a RARE and an AP-2 binding site in the regulation of the human HOX A4 gene promoter
Department of Tumor Biology, University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.
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