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Originally published In Press as doi:10.1074/jbc.M201493200 on July 26, 2002

J. Biol. Chem., Vol. 277, Issue 40, 36921-36930, October 4, 2002
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Identifying Genes Regulated in a Myc-dependent Manner*

John D. WatsonDagger §, Sara K. OsterDagger §, Mary ShagoDagger , Fereshteh KhosraviDagger , and Linda Z. PennDagger ||

From the Dagger  Ontario Cancer Institute and  Department of Medical Biophysics, University of Toronto, Toronto, Ontario M5G 2M9, Canada

The c-myc proto-oncogene can direct a diverse array of biological activities, including cell cycle progression, apoptosis, and differentiation. It is believed that Myc can affect this wide variety of activities by functioning as a regulator of gene transcription, although few targets have been identified to date. To delineate the molecular program regulated downstream of Myc, we used a cDNA microarray approach and identified 52 putative targets out of >6000 cDNAs analyzed. To further distinguish the subset of genes whose regulation was dependent upon Myc per se from those regulated in response to activation of general mitogenic or apoptotic programs, the putative cDNA targets were then screened by a series of assays. By this approach 37 putative targets were ruled out and 15 Myc target genes were uncovered. Interestingly, comparing our results with other high throughput screens reveals that certain putative Myc targets previously reported are shown not to be regulated downstream of Myc (e.g. ribosomal proteins, HSP90beta ), whereas others are further supported by our analyses (e.g. pdgfbeta r, nucleolin). The identity of genes specifically regulated downstream of Myc provides the critical tools required to understand the role Myc holds in the transformation process and to delineate how Myc functions as a regulator of gene transcription.

* This work was supported by a grant from the National Cancer Institute of Canada (NCIC) with funds from the Canadian Cancer Society (to L. Z. P.), by scholarships from the NCIC with funds from the Terry Fox Foundation (to S. K. O.), and by the Canadian Institute for Health Research (to S. K. O. and M. S.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Both authors contributed equally to this work.

|| To whom correspondence should be addressed: Division of Cellular and Molecular Biology, Ontario Cancer Institute/Princess Margaret Hospital, 610 University Ave., Toronto, Ontario M5G 2M9, Canada. Tel.: 416-946-2276; Fax: 416-946-2840; E-mail: lpenn@uhnres.utoronto.ca.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.


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