Document Type

Article

Publication Date

11-22-2005

Comments

This article has been peer-reviewed. It is the author's final version prior to publication in Mammalian Genome 17(3):189-202, March 2006. The original publication is available at http://www.springerlink.com/openurl.asp?genre=article&id=doi:10.1007/s00335-005-0066-3. Copyright is retained by Springer.

Abstract

The basis of eukaryotic complexity is an intricate genetic architecture where parallel systems are involved in tuning gene expression, via RNA-DNA, RNA-RNA and RNA-protein and DNA-protein interactions. In higher organisms, about 97% of the transcriptional output is represented by non-coding RNA (ncRNA) encompassing not only rRNA, tRNA, introns, 5’ and 3’-untranslated regions, transposable elements and intergenic regions, but also a large rapidly emerging family, named microRNAs. MicroRNAs are short 20-22 nucleotide RNA molecules that have been shown to regulate the expression of other genes in a variety of eukaryotic systems. MicroRNAs are formed from larger transcripts that fold to produce hairpin structures and serve as substrates for the cytoplasmic Dicer, a member of the RNase III enzyme family. A recent analysis of the genomic location of human microRNA genes suggested that 50% of microRNA genes are located in cancer-associated genomic regions or in fragile sites. This review focuses on the possible implications of microRNAs in post-transcriptional gene regulation in mammalian diseases, with particular focus on cancer. We argue that developing mouse models for deleted and/or overexpressed microRNAs will be of invaluable interest to decipher the regulatory networks where microRNAs are involved.

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