Nucleic Acids Research, Vol 25, Issue 10 2012-2019, Copyright © 1997 by Oxford University Press
AP Kumar and AP Butler
Ornithine decarboxylase (ODC) expression is important for proliferation and
is elevated in many tumor cells. We previously showed that Sp1 is a major
positive regulator of ODC transcription. In this paper we have investigated
transcriptional regulation of rat ODC by the closely related factor Sp3.
While over-expression of Sp1 caused a dramatic activation of the ODC
promoter, over-expression of Sp3 caused little or no activation in either
Drosophila SL2 cells (lacking endogenous Sp1 or Sp3) or in H35 rat hepatoma
cells. Furthermore, co-transfection studies demonstrated that Sp3 abolished
trans -activation of the ODC promoter by Sp1. DNase I footprint studies and
electrophoretic mobility shift assays demonstrated that both recombinant
Sp1 and Sp3 bind specifically to several sites within the ODC promoter also
protected by nuclear extracts, including overlapping GC and CT motifs
located between -116 and -104. This CT element is a site of negative ODC
regulation. Mutation of either element reduced binding, but mutation of
both sites was required to eliminate binding of either Sp1 or Sp3. These
results demonstrate that ODC is positively regulated by Sp1 and negatively
regulated by Sp3, suggesting that the ratio of these transcription factors
may be an important determinant of ODC expression during development or
transformation.
ARTICLES
Transcription factor Sp3 antagonizes activation of the ornithine decarboxylase promoter by Sp1
The University of Texas M. D. Anderson Cancer Center, Science Park- Research Division, Smithville, TX 78957, USA.
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