MYC Association with Cancer Risk and a New Model of MYC-Mediated Repression

MYC is one of the most frequently mutated and overexpressed genes in human cancer but the regulation of MYC expression and the ability of MYC protein to repress cellular genes (including itself) have remained mysterious. Recent genome-wide association studies show that many genetic polymorphisms ass...

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Published inCold Spring Harbor perspectives in medicine Vol. 4; no. 7; p. a014316
Main Author Cole, M. D.
Format Journal Article
LanguageEnglish
Published United States Cold Spring Harbor Laboratory Press 01.07.2014
Subjects
DNA Methylation - genetics
Enhancer of Zeste Homolog 2 Protein
Epigenetic Repression - genetics
Genes, myc - genetics
Genetic Predisposition to Disease - genetics
Humans
Membrane Proteins - genetics
Models, Genetic
Mutation - genetics
Neoplasms - genetics
Phosphorylation - genetics
Polycomb Repressive Complex 2 - genetics
Polymorphism, Single Nucleotide - genetics
Proto-Oncogene Proteins c-myc - genetics
Proto-Oncogene Proteins c-myc - metabolism
PTEN Phosphohydrolase - genetics
Risk Factors
Online AccessGet full text
ISSN2157-1422
2472-5412
DOI10.1101/cshperspect.a014316

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Abstract MYC is one of the most frequently mutated and overexpressed genes in human cancer but the regulation of MYC expression and the ability of MYC protein to repress cellular genes (including itself) have remained mysterious. Recent genome-wide association studies show that many genetic polymorphisms associated with disease risk map to distal regulatory elements that regulate the MYC promoter through large chromatin loops. Cancer risk-associated single-nucleotide polymorphisms (SNPs) contain more potent enhancer activity, promoting higher MYC levels and a greater risk of disease. The MYC promoter is also subject to complex regulatory circuits and limits its own expression by a feedback loop. A model for MYC autoregulation is discussed which involves a signaling pathway between the PTEN (phosphatase and tensin homolog) tumor suppressor and repressive histone modifications laid down by the EZH2 methyltransferase.
AbstractList MYC is one of the most frequently mutated and overexpressed genes in human cancer but the regulation of MYC expression and the ability of MYC protein to repress cellular genes (including itself) have remained mysterious. Recent genome-wide association studies show that many genetic polymorphisms associated with disease risk map to distal regulatory elements that regulate the MYC promoter through large chromatin loops. Cancer risk-associated single-nucleotide polymorphisms (SNPs) contain more potent enhancer activity, promoting higher MYC levels and a greater risk of disease. The MYC promoter is also subject to complex regulatory circuits and limits its own expression by a feedback loop. A model for MYC autoregulation is discussed which involves a signaling pathway between the PTEN (phosphatase and tensin homolog) tumor suppressor and repressive histone modifications laid down by the EZH2 methyltransferase.MYC is one of the most frequently mutated and overexpressed genes in human cancer but the regulation of MYC expression and the ability of MYC protein to repress cellular genes (including itself) have remained mysterious. Recent genome-wide association studies show that many genetic polymorphisms associated with disease risk map to distal regulatory elements that regulate the MYC promoter through large chromatin loops. Cancer risk-associated single-nucleotide polymorphisms (SNPs) contain more potent enhancer activity, promoting higher MYC levels and a greater risk of disease. The MYC promoter is also subject to complex regulatory circuits and limits its own expression by a feedback loop. A model for MYC autoregulation is discussed which involves a signaling pathway between the PTEN (phosphatase and tensin homolog) tumor suppressor and repressive histone modifications laid down by the EZH2 methyltransferase.
MYC is one of the most frequently mutated and overexpressed genes in human cancer but the regulation of MYC expression and the ability of MYC protein to repress cellular genes (including itself) have remained mysterious. Recent genome-wide association studies show that many genetic polymorphisms associated with disease risk map to distal regulatory elements that regulate the MYC promoter through large chromatin loops. Cancer risk-associated single-nucleotide polymorphisms (SNPs) contain more potent enhancer activity, promoting higher MYC levels and a greater risk of disease. The MYC promoter is also subject to complex regulatory circuits and limits its own expression by a feedback loop. A model for MYC autoregulation is discussed which involves a signaling pathway between the PTEN (phosphatase and tensin homolog) tumor suppressor and repressive histone modifications laid down by the EZH2 methyltransferase. The MYC promoter is subject to complex regulatory circuits. It can be regulated by distant regulatory elements; it also limits its own expression by a feedback loop.
MYC is one of the most frequently mutated and overexpressed genes in human cancer but the regulation of MYC expression and the ability of MYC protein to repress cellular genes (including itself) have remained mysterious. Recent genome-wide association studies show that many genetic polymorphisms associated with disease risk map to distal regulatory elements that regulate the MYC promoter through large chromatin loops. Cancer risk-associated single-nucleotide polymorphisms (SNPs) contain more potent enhancer activity, promoting higher MYC levels and a greater risk of disease. The MYC promoter is also subject to complex regulatory circuits and limits its own expression by a feedback loop. A model for MYC autoregulation is discussed which involves a signaling pathway between the PTEN (phosphatase and tensin homolog) tumor suppressor and repressive histone modifications laid down by the EZH2 methyltransferase.
Author Cole, M. D.
AuthorAffiliation Departments of Pharmacology and Genetics, Geisel School of Medicine at Dartmouth College, Lebanon, New Hampshire 03756
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Snippet MYC is one of the most frequently mutated and overexpressed genes in human cancer but the regulation of MYC expression and the ability of MYC protein to...
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StartPage a014316
SubjectTerms DNA Methylation - genetics
Enhancer of Zeste Homolog 2 Protein
Epigenetic Repression - genetics
Genes, myc - genetics
Genetic Predisposition to Disease - genetics
Humans
Membrane Proteins - genetics
Models, Genetic
Mutation - genetics
Neoplasms - genetics
Phosphorylation - genetics
Polycomb Repressive Complex 2 - genetics
Polymorphism, Single Nucleotide - genetics
Proto-Oncogene Proteins c-myc - genetics
Proto-Oncogene Proteins c-myc - metabolism
PTEN Phosphohydrolase - genetics
Risk Factors
Title MYC Association with Cancer Risk and a New Model of MYC-Mediated Repression
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https://pubmed.ncbi.nlm.nih.gov/PMC4066640
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