Supplementary Information for:
Transcription repression in oncogenic transformation:
Common targets of epigenetic repression in cells
transformed by Fos, Ras or Dnmt1
Jared M. Ordway¹, Katy Williams² and Tom Curran<sup>1*

1</sup>Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis TN 38105
²Department of Biology and Biochemistry, University of Bath, Claverton Down, Bath BA2 7AY, United Kingdom.

Summary
Fos and Ras function in both dependent and independent signal transduction pathways, and sustained activity of either oncogene is sufficient to induce cell transformation and tumorigenesis. Increased DNA (cytosine-5) methyltransferse (Dnmt1) activity is involved in the mechanism of transformation by both oncogenes, suggesting that inappropriate epigenetic transcription regulation may be a common route of oncogenesis. Here, we identify a common subset of differentially expressed genes in cells transformed by c-fos, v-fos, ras or Dnmt1. This cohort includes an overrepresentation of repressed genes, many of which have been functionally implicated in suppression of transformation or tumorigenesis. Furthermore, we identified four potential tumor suppressor genes subject to epigenetic transcriptional repression in transformed cells. These observations provide insights into the temporal process of DNA methylation-associated gene silencing in transformation and tumorigenesis.

*To whom correspondence should be addressed: Thomas.curran@stjude.org