Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays
Identifieur interne : 002C78 ( Main/Exploration ); précédent : 002C77; suivant : 002C79Conserved transcription factor binding sites of cancer markers derived from primary lung adenocarcinoma microarrays
Auteurs : Yee Leng Yap [République populaire de Chine, France, Hong Kong] ; Maria P. Wong [République populaire de Chine] ; Xue Wu Zhang [République populaire de Chine] ; David Hernandez [Suisse] ; Robin Gras [Suisse] ; David K. Smith [République populaire de Chine] ; Antoine Danchin [France]Source :
- Nucleic Acids Research [ 0305-1048 ] ; 2005.
Abstract
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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DOI: 10.1093/nar/gki188
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Acids Res.</title><idno type="ISSN">0305-1048</idno><idno type="eISSN">1362-4962</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2005">2005</date><biblScope unit="volume">33</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="409">409</biblScope><biblScope unit="page" to="421">421</biblScope></imprint><idno type="ISSN">0305-1048</idno></series><idno type="istex">0BFC1DB5DBE0149707002F146869EB08D51A995C</idno><idno type="DOI">10.1093/nar/gki188</idno><idno type="local">gki188</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0305-1048</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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. 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