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Volume 272, Number 52, Issue of December 26, 1997
pp. 33181-33190
(Received for publication, August 6, 1997)
From the Cyclin D1 is a critical oncogene involved in the
regulation of progression through the G1 phase of the
cell cycle, thereby contributing to cell proliferation. This is
mediated through interaction of cyclin D1 with its catalytic partners,
the cyclin-dependent kinases, and the subsequent
phosphorylation of the retinoblastoma protein. Cyclin D1, in turn, is
regulated by mitogenic stimuli. We demonstrate that transforming growth
factor-
Transforming Growth Factor-
Enhances Cyclin D1 Transcription
through the Binding of Early Growth Response Protein to a
cis-Regulatory Element in the Cyclin D1 Promoter
,
,¶
Gastrointestinal Unit and the
¶ Hematology-Oncology Unit, Department of Medicine, Massachusetts
General Hospital, Harvard Medical School, Boston, Massachusetts 02114 and the § Pulmonary Division, Department of Medicine, Boston
University School of Medicine, Boston, Massachusetts 02114
(TGF) induces cyclin D1 mRNA in esophageal squamous
epithelial cells, and this appears to correlate with increased cyclin
D1 protein expression and cyclin-dependent kinase 6 activity. The induction of cyclin D1 transcription by TGF is
mediated in part through the induction of the early growth response
protein (Egr-1) and its subsequent binding of Egr-1 to a
cis-regulatory region spanning nucleotides 
144 to 104
of the cyclin D1 promoter. The Egr-1 binding activity to the cyclin D1
promoter appears to require de novo protein synthesis and
is not influenced by Sp1 binding to overlapping Sp1 motifs. Taken
together, these data provide evidence that TGF enhances cyclin D1
transcription through the induction of Egr-1 binding to a
cis-regulatory region in the cyclin D1 promoter. This has important mechanistic implications into the transcriptional regulation of cyclin D1 by an essential proproliferative growth factor and cell
cycle progression.
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