c-Myc promoter activation in medulloblastoma

%The c-myc oncogene is commonly activated in medulloblastoma. Genomic amplification is a well-documented cause of c-myc activation but does not account for all cases of c-myc activation. In this study, we sought other means by which c-myc is overexpressed in medulloblastoma. Twelve medulloblastoma o...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 2003-08, Vol.63 (16), p.4773-4776
Main Authors: SIU, I-Mei, LAL, Anita, BLANKENSHIP, Jill R, ALDOSARI, Naji, RIGGINS, Gregory J
Format: Article
Language:English
Subjects:
b-catenin
Base Sequence
beta Catenin
Binding Sites
Biological and medical sciences
c-myc gene
Cytoskeletal Proteins - metabolism
Gene Expression Regulation, Neoplastic
General aspects (metabolism, cell proliferation, established cell line...)
Genes, myc
Humans
Medical sciences
medulloblastoma
Medulloblastoma - genetics
Molecular Sequence Data
Promoter Regions, Genetic
Trans-Activators - metabolism
Tumor cell
Tumor Cells, Cultured
Tumors
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Summary:%The c-myc oncogene is commonly activated in medulloblastoma. Genomic amplification is a well-documented cause of c-myc activation but does not account for all cases of c-myc activation. In this study, we sought other means by which c-myc is overexpressed in medulloblastoma. Twelve medulloblastoma or PNET cell lines were screened for c-myc genomic amplification, mRNA levels, and protein levels. Two medulloblastoma lines, D283 Med and D721 Med, were identified that expressed c-myc mRNA and protein at high levels without genomic amplification. The c-myc gene's regulatory sequences were normal in those cell lines. However, specific regions of the promoter, independent of the beta-catenin binding sites, were responsible for activation as revealed by promoter assays and site-directed mutagenesis. Transcriptional activation by a beta-catenin-independent pathway is therefore a likely mechanism for c-myc overexpression in a subset of medulloblastomas.
ISSN:0008-5472
1538-7445