TY - JOUR
T1 - The c-Myc target gene network
AU - Dang, Chi V.
AU - O'Donnell-Mendell, Kathryn A
AU - Zeller, Karen I.
AU - Nguyen, Tam
AU - Osthus, Rebecca C.
AU - Li, Feng
N1 - Funding Information:
We apologize for omissions due to space limitation. We thank J. Mendell and members of the Dang Laboratory for their comments. Our original work is supported by NCI grants CA51497 and CA57341. CVD is Johns Hopkins Family Professor in Oncology Research.
PY - 2006/8
Y1 - 2006/8
N2 - For more than a decade, numerous studies have suggested that the c-Myc oncogenic protein is likely to broadly influence the composition of the transcriptome. However, the evidence required to support this notion was made available only recently, much to the anticipation of an eagerly awaiting field. In the past 5 years, many high-throughput screens based on microarray gene expression profiling, serial analysis of gene expression (SAGE), chromatin immunoprecipitation (ChIP) followed by genomic array analysis, and Myc-methylase chimeric proteins have generated a wealth of information regarding Myc responsive and target genes. From these studies, the c-Myc target gene network is estimated to comprise about 15% of all genes from flies to humans. Both genomic and functional analyses of c-Myc targets suggest that while c-Myc behaves as a global regulator of transcription, groups of genes involved in cell cycle regulation, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function are over-represented in the c-Myc target gene network. c-Myc also consistently represses genes involved in cell growth arrest and cell adhesion. The overexpression of c-Myc predisposes cells to apoptosis under nutrient or growth factor deprivation conditions, although the critical sets of genes involved remain elusive. Despite tremendous advances, the downstream target genes that distinguish between physiologic and tumorigenic functions of c-Myc remain to be delineated.
AB - For more than a decade, numerous studies have suggested that the c-Myc oncogenic protein is likely to broadly influence the composition of the transcriptome. However, the evidence required to support this notion was made available only recently, much to the anticipation of an eagerly awaiting field. In the past 5 years, many high-throughput screens based on microarray gene expression profiling, serial analysis of gene expression (SAGE), chromatin immunoprecipitation (ChIP) followed by genomic array analysis, and Myc-methylase chimeric proteins have generated a wealth of information regarding Myc responsive and target genes. From these studies, the c-Myc target gene network is estimated to comprise about 15% of all genes from flies to humans. Both genomic and functional analyses of c-Myc targets suggest that while c-Myc behaves as a global regulator of transcription, groups of genes involved in cell cycle regulation, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function are over-represented in the c-Myc target gene network. c-Myc also consistently represses genes involved in cell growth arrest and cell adhesion. The overexpression of c-Myc predisposes cells to apoptosis under nutrient or growth factor deprivation conditions, although the critical sets of genes involved remain elusive. Despite tremendous advances, the downstream target genes that distinguish between physiologic and tumorigenic functions of c-Myc remain to be delineated.
KW - Myc
KW - Target genes
KW - Transcription
KW - Tumorigenesis
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U2 - 10.1016/j.semcancer.2006.07.014
DO - 10.1016/j.semcancer.2006.07.014
M3 - Review article
C2 - 16904903
AN - SCOPUS:33748171960
SN - 1044-579X
VL - 16
SP - 253
EP - 264
JO - Seminars in Cancer Biology
JF - Seminars in Cancer Biology
IS - 4
ER -