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      An integrated database of genes responsive to the Myc oncogenic transcription factor: identification of direct genomic targets

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          A database of genes responsive to the c-Myc oncogenic transcription factor is described. The database Myc Target Gene prioritizes candidate target genes according to experimental evidence and clusters responsive genes into functional groups.

          Abstract

          We report a database of genes responsive to the Myc oncogenic transcription factor. The database Myc Target Gene prioritizes candidate target genes according to experimental evidence and clusters responsive genes into functional groups. We coupled the prioritization of target genes with phylogenetic sequence comparisons to predict c-Myc target binding sites, which are in turn validated by chromatin immunoprecipitation assays. This database is essential for the understanding of the genetic regulatory networks underlying the genesis of cancers.

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          MYC oncogenes and human neoplastic disease.

          C Nesbit, J. Tersak, E Prochownik (1999)
          c-myc, N-myc and L-myc are the three members of the myc oncoprotein family whose role in the pathogenesis of many human neoplastic diseases has received wide empirical support. In this review, we first summarize data, derived mainly from non-clinical studies, indicating that these oncoproteins actually serve quite different roles in vivo. This concept necessarily lies at the heart of the basis for the observation that the deregulated expression of each MYC gene is reproducibly associated with only certain naturally occurring malignancies in humans and that these genes are not interchangeable with respect to their aberrant functional consequences. We also review evidence implicating each of the above MYC genes in specific neoplastic diseases and have attempted to identify unresolved questions which deserve further basic or clinical investigation. We have made every attempt to review those diseases for which significant and confirmatory evidence, based on studies with primary tumor material, exists to implicate MYC members in their causation and/or progression.
          Article 0 comments Cited 266 times – based on 0 reviews     Review now
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            A global transcriptional regulatory role for c-Myc in Burkitt's lymphoma cells.

            Zirong Li, Sara Van Calcar, Chunxu Qu … (2003)
            Overexpression of c-Myc is one of the most common alterations in human cancers, yet it is not clear how this transcription factor acts to promote malignant transformation. To understand the molecular targets of c-Myc function, we have used an unbiased genome-wide location-analysis approach to examine the genomic binding sites of c-Myc in Burkitt's lymphoma cells. We find that c-Myc together with its heterodimeric partner, Max, occupy >15% of gene promoters tested in these cancer cells. The DNA binding of c-Myc and Max correlates extensively with gene expression throughout the genome, a hallmark attribute of general transcription factors. The c-Myc/Max heterodimer complexes also colocalize with transcription factor IID in these cells, further supporting a general role for overexpressed c-Myc in global gene regulation. In addition, transcription of a majority of c-Myc target genes exhibits changes correlated with levels of c-myc mRNA in a diverse set of tissues and cell lines, supporting the conclusion that c-Myc regulates them. Taken together, these results suggest a general role for overexpressed c-Myc in global transcriptional regulation in some cancer cells and point toward molecular mechanisms for c-Myc function in malignant transformation.
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              Binding of c-Myc to chromatin mediates mitogen-induced acetylation of histone H4 and gene activation.

              S Taubert, Thomas S Frank, Charles M. Schroeder … (2001)
              The Myc protein binds DNA and activates transcription by mechanisms that are still unclear. We used chromatin immunoprecipitation (ChIP) to evaluate Myc-dependent changes in histone acetylation at seven target loci. Upon serum stimulation of Rat1 fibroblasts, Myc associated with chromatin, histone H4 became locally hyperacetylated, and gene expression was induced. These responses were lost or severely impaired in Myc-deficient cells, but were restored by adenoviral delivery of Myc simultaneous with mitogenic stimulation. When targeted to chromatin in the absence of mitogens, Myc directly induced H4 acetylation. In addition, Myc recruited TRRAP to chromatin, consistent with a role for this cofactor in histone acetylation. Finally, unlike serum, Myc alone was very inefficient in inducing expression of most target genes. Myc therefore governs a step, most likely H4 acetylation, that is required but not sufficient for transcriptional activation. We propose that Myc acts as a permissive factor, allowing additional signals to activate target promoters.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Genome Biol
                Title: Genome Biology
                Publisher: BioMed Central (London )
                ISSN (Print): 1465-6906
                ISSN (Electronic): 1465-6914
                Publication date (Print): 2003
                Publication date (Electronic): 11 September 2003
                Volume: 4
                Issue: 10
                Page: R69
                Affiliations
                [1 ]Division of Hematology, Department of Medicine, The Sidney Kimmel Comprehensive Cancer Center, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
                [2 ]Divisions of Pediatric Informatics and Molecular Developmental Biology, Children's Hospital Research Foundation, Children's Hospital Medical Center and Department of Biomedical Engineering, University of Cincinnati, Cincinnati, OH 45229, USA
                [3 ]Program in Human Genetics and Molecular Biology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
                Article
                Publisher ID: gb-2003-4-10-r69
                DOI: 10.1186/gb-2003-4-10-r69
                PMC ID: 328458
                PubMed ID: 14519204
                SO-VID: d69f5dda-73f9-4af8-b048-3060b3a5d074
                Copyright © Copyright © 2003 Zeller et al.; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
                History
                Date received : 17 June 2003
                Date revision received : 18 July 2003
                Date accepted : 5 August 2003
                Categories
                Subject: Software

                ScienceOpen disciplines: Genetics
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                ScienceOpen disciplines: Genetics

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