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Nucleic Acids Research 2005 33(1):409-421; doi:10.1093/nar/gki188
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Published online 14 January 2005

© 2005, the authors Nucleic Acids Research, Vol. 33 No. 1 © Oxford University Press 2005; all rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use permissions, please contact journals.permissions{at}oupjournals.org.

Article

Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays

Yee Leng Yap1,2,*, Maria P. Wong3, Xue Wu Zhang1, David Hernandez4, Robin Gras4, David K. Smith5 and Antoine Danchin2

1 HKU-Pasteur Research Centre Dexter H.C. Man Building, 8 Sassoon Road Pokfulam, Hong Kong, China 2 Institute Pasteur, Unité de Génétique des Génomes Bactériens CNRS URA 2171, 28 rue du Docteur Roux, 75724 Paris Cedex 15, France 3 Department of Pathology, The University of Hong Kong Pokfulam, Hong Kong, China 4 Swiss Institute of Bioinformatics Proteome Informatics Group, CMU 1 Rue Michel-Servet CH 1211, Geneva 4, Switzerland 5 Department of Biochemistry, The University of Hong Kong Pokfulam, Hong Kong, China

*To whom correspondence should be addressed at HKU-Pasteur Research Centre, 8, Sassoon Road, Pokfulam, HongKong, China. Tel: +852 2816 8438; Fax: +852 2872 5782; Email: daniely{at}hkusua.hku.hk

Received August 14, 2004. Revised November 2, 2004. Accepted December 12, 2004.

Gene transcription in a set of 49 human primary lung adenocarcinomas and 9 normal lung tissue samples was examined using Affymetrix GeneChip technology. A total of 3442 genes, called the set M AD, were found to be either up- or down-regulated by at least 2-fold between the two phenotypes. Genes assigned to a particular gene ontology term were found, in many cases, to be significantly unevenly distributed between the genes in and outside M AD. Terms that were overrepresented in M AD included functions directly implicated in the cancer cell metabolism. Based on their functional roles and expression profiles, genes in M AD were grouped into likely co-regulated gene sets. Highly conserved sequences in the 5 kb region upstream of the genes in these sets were identified with the motif discovery tool, MoDEL. Potential oncogenic transcription factors and their corresponding binding sites were identified in these conserved regions using the TRANSFAC 8.3 database. Several of the transcription factors identified in this study have been shown elsewhere to be involved in oncogenic processes. This study searched beyond phenotypic gene expression profiles in cancer cells, in order to identify the more important regulatory transcription factors that caused these aberrations in gene expression.


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