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Molecular and Cellular Biology, December 2001, p. 8428-8436, Vol. 21, No. 24
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.24.8428-8436.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

The Putative Oncoprotein Bcl-3 Induces Cyclin D1 To Stimulate G1 Transition

Sandy D. Westerheide,1 Marty W. Mayo,1,dagger Vasiliki Anest,1,2 Julie L. Hanson,1,2 and Albert S. Baldwin Jr.1,2,3,*

Lineberger Comprehensive Cancer Center,1 Curriculum in Genetics and Molecular Biology,2 and Department of Biology,3 University of North Carolina, Chapel Hill, North Carolina 27599

Received 3 July 2001/Returned for modification 7 August 2001/Accepted 20 September 2001

Bcl-3 is a distinctive member of the Ikappa B family of NF-kappa B inhibitors because it can function to coactivate transcription. A potential involvement of Bcl-3 in oncogenesis is highlighted by the fact that it was cloned due to its location at a breakpoint junction in some cases of human B-cell chronic lymphocytic leukemia and that it is highly expressed in human breast tumor tissue. To analyze the effects of Bcl-3 dysregulation in breast epithelial cells, we created stable immortalized human breast epithelial cell lines either expressing Bcl-3 or carrying the corresponding vector control plasmid. Analysis of the Bcl-3-expressing cells suggests that these cells have a shortened G1 phase of the cell cycle as well as a significant increase in hyperphosphorylation of the retinoblastoma protein. Additionally, the cyclin D1 gene was found to be highly expressed in these cells. Upon further analysis, Bcl-3, acting as a coactivator with NF-kappa B p52 homodimers, was demonstrated to directly activate the cyclin D1 promoter through an NF-kappa B binding site. Therefore, our results demonstrate that dysregulated expression of Bcl-3 potentiates the G1 transition of the cell cycle by stimulating the transcription of the cyclin D1 gene in human breast epithelial cells.

* Corresponding author. Mailing address: Lineberger Comprehensive Cancer Center, Campus Box 7295, University of North Carolina, Chapel Hill, NC 27599. Phone: (919) 966-3652. Fax: (919) 966-0444. E-mail: jhall{at}med.unc.edu.

dagger Present address: Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA 22908.

Molecular and Cellular Biology, December 2001, p. 8428-8436, Vol. 21, No. 24
0270-7306/01/$04.00+0   DOI: 10.1128/MCB.21.24.8428-8436.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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