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Molecular Signaling and Oncogenesis Section, Department of Cancer and Cell Biology, Medicine Branch, Division of Clinical Science, National Cancer Institute, Bethesda, Maryland 20892 [Q. M. G., C. C., M. H., M. R., K. S., E. T. L.]; Department of Molecular and Cellular Biology, The Institute for Genomic Research, Rockville, Maryland 20850 [R. L. M., N. H. L.]; and Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [S. K., C. V. D.]
c-Myc functions through direct activation or repression of transcription. Using cDNA microarray analysis, we have identified c-Myc-responsive genes by comparing gene expression profiles between c-myc null and c-myc wild-type rat fibroblast cells and between c-myc null and c-myc null cells reconstituted with c-myc. From a panel of 4400 cDNA elements, we found 198 genes responsive to c-myc when comparing wild-type or reconstituted cells with the null cells. The plurality of the named c-Myc-responsive genes that were up-regulated, including 30 ribosomal protein genes, are involved in macromolecular synthesis and metabolism, suggesting a major role of c-Myc in the regulation of protein synthetic and metabolic pathways. When ectopically overexpressed, c-Myc induced a different and smaller set of c-Myc-responsive genes as compared with the physiologically expressed c-Myc condition. Thus, these results from expression profiling suggest a new primary function for c-Myc and raise the possibility that the physiological and transforming functions of c-myc may be separable.
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