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J. Biol. Chem., Vol. 282, Issue 13, 9703-9712, March 30, 2007

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Identification of Genes Directly Regulated by the Oncogene ZNF217 Using Chromatin Immunoprecipitation (ChIP)-Chip Assays^*

Sheryl R. Krig¹², Victor X. Jin¹, Mark C. Bieda, Henriette O'Geen, Paul Yaswen, Roland Green^¶, and Peggy J. Farnham³

From the Department of Pharmacology and the Genome Center, University of California, Davis, California 95616, ^¶NimbleGen Systems Inc., Madison, Wisconsin 53711, and Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720

It has been proposed that ZNF217, which is amplified at 20q13 in various tumors, plays a key role during neoplastic transformation. ZNF217 has been purified in complexes that contain repressor proteins such as CtBP2, suggesting that it acts as a transcriptional repressor. However, the function of ZNF217 has not been well characterized due to a lack of known target genes. Using a global chromatin immunoprecipitation (ChIP)-chip approach, we identified thousands of ZNF217 binding sites in three tumor cell lines (MCF7, SW480, and Ntera2). Further analysis of ZNF217 in Ntera2 cells showed that many promoters are bound by ZNF217 and CtBP2 and that a subset of these promoters are activated upon removal of ZNF217. Thus, our in vivo studies corroborate the in vitro biochemical analyses of ZNF217-containing complexes and support the hypothesis that ZNF217 functions as a transcriptional repressor. Gene ontology analysis showed that ZNF217 targets in Ntera2 cells are involved in organ development, suggesting that one function of ZNF217 may be to repress differentiation. Accordingly we show that differentiation of Ntera2 cells with retinoic acid led to down-regulation of ZNF217. Our identification of thousands of ZNF217 target genes will enable further studies of the consequences of aberrant expression of ZNF217 during neoplastic transformation.

Received for publication, December 22, 2006 , and in revised form, January 25, 2007.

^* This work was supported in part by Public Health Service Grants CA45250, HG003129, and DK067889. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplemental Fig. S1 and Tables S1–S7.

¹ Both authors contributed equally to this work.

² Supported by California Breast Cancer Research Program Postdoctoral Fellowship Grant 11FB-0029.

³ To whom correspondence should be addressed: Dept. of Pharmacology and the Genome Center, University of California, One Shields Ave., Davis, CA 95616. Tel.: 530-754-4988; Fax: 530-752-0436; E-mail: pjfarnham{at}ucdavis.edu.

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