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Molecular Biology, Pathobiology, and Genetics |
1 Institute for Cancer Genetics, 2 Department of Pathology and Cell Biology, 3 Columbia Genome Center, 4 Department of Medicine, and 5 Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York; and 6 Department of Obstetrics and Gynecology, Tohoku University School of Medicine, Seiryo-machi, Aoba-ku, Sendai, Miyagi, Japan
Requests for reprints: Ramon Parsons, Columbia University ICRC406, 1130 St. Nicholas Avenue, New York, NY 10032. Phone: 212-851-5278; Fax: 212-851-5267; E-mail: rep15{at}columbia.edu.
Key Words: BAF180 PB1 p21/WAF1/CIP1 tumor suppressor breast cancer
Screening for tumor suppressor genes in breast cancer revealed multiple truncating mutations of PB1, which encodes the BAF180 subunit of the PBAF chromatin remodeling complex. Mutation was associated with loss of heterozygosity of the wild-type allele. BAF180 complementation of BAF180-mutant tumor cells caused G1 arrest that was dependent on increased expression of the cyclin/cyclin-dependent kinase inhibitor p21/WAF1/CIP1. Endogenous wild-type BAF180 bound to the p21 promoter and was required for proper p21 expression and G1 arrest after transforming growth factor-β and
-radiation treatment. BAF180 thus functions on two tumor suppressor signaling pathways as a physiologic mediator of p21 expression. We conclude that BAF180 suppresses tumorigenesis, at least in part, through its ability to regulate p21. [Cancer Res 2008;68(6):1667–74]
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