Review

The Pharmacogenomics Journal (2007) 7, 297–304; doi:10.1038/sj.tpj.6500429; published online 26 December 2006

Molecular therapy in the microRNA era

T Wurdinger1,2 and F F Costa1,3

  1. 1Molecular Neurogenetics Unit, Massachusetts General Hospital and Harvard Medical School, Boston/Charlestown, MA, USA
  2. 2Center for Molecular Imaging Research, Massachusetts General Hospital and Harvard Medical School, Boston/Charlestown, MA, USA
  3. 3Cancer Biology and Epigenomics Program, Children's Memorial Research Center and Northwestern University's Feinberg School of Medicine, 2300 Children's Plaza, Chicago, IL, USA

Correspondence: Dr FF Costa, Cancer Biology and Epigenomics Program, Children's Memorial Research Center and Northwestern University's Feinberg School of Medicine, 2300 Children's Plaza, Box 220, Chicago, IL, USA. E-mail: fcosta@childrensmemorial.org; T Wurdinger, E-mail: twurdinger@partners.org

Received 10 April 2006; Accepted 10 December 2006; Published online 26 December 2006.

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Abstract

MicroRNAs (miRNAs) consist of a growing class of non-coding RNAs (ncRNAs) that negatively regulate the expression of genes involved in development, differentiation, proliferation, apoptosis and other important cellular processes. miRNAs are usually 18–25 nt long and are each able to regulate several mRNAs by mechanisms such as incomplete base pairing and Post-Transcriptional Gene Silencing (PTGS). A growing number of reports have shown that aberrant miRNA expression is a common feature of human diseases including cancer, which has sparked interest in targeting these regulators of gene expression as a means of ameliorating these diseases. Here, we review important aspects of miRNA function in normal and pathological states and discuss new modalities of epigenetic intervention strategies that could be used to amend defects in miRNA/mRNA interactions.

Keywords:

non-coding RNAs, miRNAs, mRNA targets, multigenic diseases, cancer, 'epigenetic' therapy

Abbreviations:

AMOs, anti-miRNA oligonucleotides; CMV, Cytomegalovirus; hAT1R, Angiotensin II Type 1 receptor; HDAC4, Histone deacetylase 4; LNAs, Locked nucleic acid anti-sense oligonucleotides; miRNAs, microRNAs; ncRNAs, non-coding RNAs; pre-miRNAs, precursor miRNAs; pri-miRNAs, primary miRNAs; PTGS, Post-Trancriptional Gene Silencing; RISC, RNA Induced Silencing Complex; RNAi, RNA interference; SRF, Serum Response Factor; shRNAs, short hairpin RNAs; siRNAs, small interfering RNAs; UTR, Untranslated Region

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