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Review
. 2017 May 4;14(5):522-535.
doi: 10.1080/15476286.2016.1172756. Epub 2016 May 26.

Long non-coding RNA: Functional agent for disease traits

Affiliations
Review

Long non-coding RNA: Functional agent for disease traits

Sriyans Jain et al. RNA Biol. .

Abstract

In recent years, long non-coding RNAs (lncRNAs) have attracted the attention of researchers with their involvement in all facets of life. LncRNAs are transcripts of more than 200 nucleotides which lack defined protein coding potential. Although they do not code for proteins, a large number of them are involved in regulating gene expression and translation. The presence of numerous lncRNAs in the human genome has prompted us to investigate the contribution of these molecules to human biology and medicine. In this review, we present the potential role of lncRNAs interlinked to different human diseases and genetic disorders. We also describe their role in cellular differentiation and aging and discuss their potential importance as biomarkers and as therapeutic agents.

Keywords: Biomarkers; epigenetics; gene regulation; human diseases; long non-coding RNA; therapeutic agents.

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Figures

Figure 1.
Figure 1.
Different mechanisms of functions associated with lncRNAs. They serve in (A) Chromatin modulation, (B) Transcriptional activation and suppression, (C) as post transcriptional machinery, (D) miRNA decoy element and (E) as protein inhibitor (Modified from Cheetham et al. 2013 Br J Cancer, 108:2419-25).
Figure 2.
Figure 2.
LncRNAs secreted from various endocrine tissues. Tissues are labeled in bold and the involved lncRNAs are also noted. (Modified from Knoll et al. 2015 Nat Rev Endocrinol, 11:151–60).
Figure 3.
Figure 3.
Misexpression of different lncRNAs in cancer that modulate different pathways with diversified mechanisms (A) a group of lncRNAs (e. g. HOTAIR, ANRIL and others) modulate chromatin structure and organization in cis or in trans (PRC2) to alter their expression (B) A group of lncRNAs induced p53 regulated pathway. The lncRNA once activated modulated via different protein partners. (Modified from Niland et al. 2012 Front Genet 3:25).

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