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Papers In Press, published online ahead of print September 10, 2002
Surgery Dept., Thomas Jefferson University, Philadelphia, PA 19107
Corresponding Author: ronald.weigel{at}mail.tju.edu
The AP2 transcription factor family is a set of developmentally regulated, retinoic acid inducible genes composed of four related factors—AP2
J. Biol. Chem, 10.1074/jbc.M208924200
Submitted on August 30, 2002
Revised on September 10, 2002
Accepted on September 10, 2002
Tumor suppressor activity of AP2
mediated through a direct interaction with p53
, AP2
, AP2
and AP2
. AP2 factors orchestrate a variety of cell processes including apoptosis, cell growth and tissue differentiation during embryogenesis. In studies of primary malignancies, AP2 has been shown to function as a tumor suppressor in breast cancer, colon cancer and malignant melanoma. In cell culture models, overexpression of AP2 inhibits cell division and stable colony formation, whereas, a dominant-negative AP2 mutant increases invasiveness and tumorigenecity. Here we show that AP2 targets the p53 tumor suppressor protein. Studies with chromatin immunoprecipitation demonstrate that AP2 is brought to p53 binding sites in p53-regulated promoters. The interaction between AP2 and p53 augments p53-mediated transcriptional activation, which results in up-regulation of the cyclin-dependent kinase inhibitor p21WAF1/CIP1. AP2 is able to induce G1 and G2 cell cycle arrest only in the presence of wild-type p53. Thus, we conclude that the tumor suppressor activity of AP2 is mediated through a direct interaction with p53. These results also provide a mechanism to explain patterns of gene expression in cancers where AP2 is known to function as a tumor suppressor.
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