Cellular epigenetic stability and cancer.
When a cell divides, it must not only accurately duplicate its genome, but also restore its previous levels of gene expression. The information determining gene expression is often not directly encoded in the DNA and is hence termed 'epigenetic'. The molecular basis of epigenetic memory remains a subject of intense debate, but is likely to arise from the collaboration of several mechanisms, including histone post-translational modifications, transcription factors, DNA methylation and noncoding RNAs. In this article, we look at how these mechanisms interact to generate robust epigenetic states. We then consider recent observations that mitotic inheritance of stable gene expression can be compromised by interruption of DNA replication. We discuss how these data may provide direct evidence for a central role for histone modifications in transcriptional memory and how they could potentially provide an explanation for the some of the widespread alterations in transcription seen in cancer cells.
Medical Research Council Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry, Hills Road, Cambridge, CB2 0QH, UK.
Peter
P
Sarkies
Julian E
JE
Sale
D000818:Animals; D044127:Epigenesis, Genetic; D006657:Histones / Q000378:metabolism; D006801:Humans; D009369:Neoplasms / Q000235:genetics*; D011499:Protein Processing, Post-Translational; D014158:Transcription, Genetic
D006657:Histones