Transcriptional regulation of a metastasis suppressor gene by Tip60 and β-catenin complexes

Jung Hwa Kim, Bogyou Kim, Ling Cai, Hee June Choi, Kenneth A. Ohgi, Chris Tran, Charlie Chen, Chin Ha Chung, Otmar Huber, David W. Rose, Charles L. Sawyers, Michael G. Rosenfeld () and Sung Hee Baek ()
Additional contact information
Jung Hwa Kim: Seoul National University
Bogyou Kim: Seoul National University
Ling Cai: Howard Hughes Medical Institute, University of California
Hee June Choi: Seoul National University
Kenneth A. Ohgi: Howard Hughes Medical Institute, University of California
Chris Tran: University of California, Los Angeles
Charlie Chen: University of California, Los Angeles
Chin Ha Chung: Seoul National University
Otmar Huber: Charite - Campus Benjamin Franklin
David W. Rose: School of Medicine, University of California, San Diego
Charles L. Sawyers: University of California, Los Angeles
Michael G. Rosenfeld: Howard Hughes Medical Institute, University of California
Sung Hee Baek: Seoul National University

Nature, 2005, vol. 434, issue 7035, 921-926

Abstract: Abstract Defining the molecular strategies that integrate diverse signalling pathways in the expression of specific gene programmes that are critical in homeostasis and disease remains a central issue in biology. This is particularly pertinent in cancer biology because downregulation of tumour metastasis suppressor genes is a common occurrence1,2, and the underlying molecular mechanisms are not well established. Here we report that the downregulation of a metastasis suppressor gene, KAI1, in prostate cancer cells involves the inhibitory actions of β-catenin, along with a reptin chromatin remodelling complex. This inhibitory function of β-catenin–reptin requires both increased β-catenin expression and recruitment of histone deacetylase activity. The coordinated actions of β-catenin–reptin components that mediate the repressive state serve to antagonize a Tip60 coactivator complex3,4,5,6,7,8 that is required for activation; the balance of these opposing complexes controls the expression of KAI1 and metastatic potential. The molecular mechanisms underlying the antagonistic regulation of β-catenin–reptin and the Tip60 coactivator complexes for the metastasis suppressor gene, KAI1, are likely to be prototypic of a selective downregulation strategy for many genes, including a subset of NF-κB target genes.

Date: 2005
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DOI: 10.1038/nature03452

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