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Basic fibroblast growth factor transcriptional autoregulation requires EGR-1
D Wang1, M W Mayo, A S Baldwin
1Lineberger Comprehensive Cancer Center and Department of Biology, University of North Carolina, Chapel Hill 27599-7295, USA.
Oncogene
|May 15, 1997
Summary
Basic fibroblast growth factor (bFGF) drives its own expression through a transcriptional process. This autoregulation relies on the transcription factor Egr-1, which binds to the bFGF promoter to control gene activity.
Area of Science:
- Molecular Biology
- Cell Biology
- Oncology
Background:
- Basic fibroblast growth factor (bFGF) promotes cell growth and angiogenesis.
- bFGF is implicated in tumorigenesis, particularly in human gliomas, where its expression is critical.
- Previous studies indicated bFGF can increase its own mRNA levels.
Purpose of the Study:
- To elucidate the mechanism by which bFGF autoregulates its own synthesis.
- To identify the key transcription factors involved in bFGF autoregulation.
Main Methods:
- Investigated the transcriptional regulation of the bFGF gene.
- Utilized mutation analysis of DNA elements within the bFGF promoter.
- Assessed the role of the transcription factor Egr-1 in bFGF gene expression.
Main Results:
- bFGF induces its own synthesis via an autoregulated transcriptional response.
- The transcription factor Egr-1 is essential for this autoregulation.
- Egr-1 binds to two specific DNA elements in the bFGF promoter, positively regulating transcription.
- Mutating these Egr-1 binding sites abrogates bFGF's ability to upregulate the bFGF promoter.
Conclusions:
- bFGF autoregulation occurs at the transcriptional level, mediated by Egr-1.
- Egr-1 acts as a crucial transcription factor, binding the bFGF promoter to control gene expression.
- This mechanism provides insight into how bFGF maintains its own expression levels.