Abstract
The recent discovery of thousands of long non-coding (lnc)RNAs in the human genome has prompted investigation of the potential roles of these molecules in human biology and medicine. Indeed, it is now well documented that many lncRNAs are involved in key biological processes, including dosage compensation, genomic imprinting, chromatin regulation, alternative splicing of pre-mRNA, nuclear organization; and potentially many other biological processes, which are yet to be elucidated. Recently, a number of studies have also reported that lncRNAs are dysregulated in a number of human diseases, including several cancers and neurological disorders. Although many of these studies have fallen short of implicating lncRNAs as causative, they suggest potential roles that warrant further in depth investigations. In this review, we discuss the current state of knowledge regarding the roles of lncRNAs in cancer and neurological disorders, and suggest potential future directions in this rapidly emerging field.
Highlights
A number of studies over the past decade have shown that mammalian genomes encode thousands of long non-coding RNAs, which are mRNA-like transcripts that lack proteincoding capacity
In addition to protein-coding genes, the expression, and/or function of several long non-coding RNAs (lncRNAs) have been shown to be affected by trinucleotide repeats raising the possibility that these lncRNAs may contribute to the disease phenotype. Both Khalil et al (2008) and Ladd et al (2007) reported the discovery of two lncRNAs, FMR4, and ASFMR1 that are expressed from the fragile X mental retardation 1 gene (FMR1) locus; which is associated with fragile X syndrome (FXS), fragile X tremor ataxia syndrome (FXTAS), and potentially autism (Penagarikano et al, 2007; Gallagher and Hallahan, 2011; Sokol et al, 2011)
CONCLUDING REMARKS It is evident that lncRNAs play important roles in many key biological processes, their mechanisms of action are yet to be fully elucidated
Summary
A number of studies over the past decade have shown that mammalian genomes encode thousands of long non-coding RNAs (lncRNAs), which are mRNA-like transcripts that lack proteincoding capacity. Perhaps interesting is the tangled web of several lncRNAs that are involved in this process by regulating the expression and action of Xist (Lee et al, 1999; Ogawa and Lee, 2003) Another lncRNA, termed HOTAIR, was shown to regulate the expression of hundreds of genes genome-wide in trans (Rinn et al, 2007; Khalil et al, 2009; Gupta et al, 2010; Tsai et al, 2010). In vitro studies have shown that over-expression of HOTAIR in cell lines leads to the recruitment of the repressive complex PRC2 to over 800 additional loci genome-wide including tumor suppressor genes (Gupta et al, 2010). The induction of specific lncRNAs by p53 that leads to gene repression could be part of the mechanism by which p53 represses
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