The contribution of long non-coding RNAs in Inflammatory Bowel Diseases

Dig Liver Dis. 2017 Oct;49(10):1067-1072. doi: 10.1016/j.dld.2017.08.003. Epub 2017 Aug 9.

Abstract

Inflammatory bowel diseases (IBDs) are multifactorial autoimmune diseases with growing prevalence but the interaction between genetic, environmental and immunologic factors in their development is complex and remains obscure. There is great need to understand their pathogenetic mechanisms and evolve diagnostic and therapeutic tools. Long non-coding RNAs (lncRNAs) are RNA molecules longer than 200 nucleotides that are known to interfere in gene regulation but their roles and functions have not yet been fully understood. While they are widely investigated in cancers, little is known about their contribution in other diseases. There is growing evidence that lncRNAs play critical role in regulation of immune system and that they interfere in the pathogenetic mechanisms of autoimmune diseases, like IBDs. Recent studies have identified lncRNAs in the proximity of IBD-associated genes and single nucleotide polymorphisms within IBD-associated lncRNAs as well. Furthermore, blood samples and pinch biopsies were also analyzed and a plethora of lncRNAs are found to be deregulated in Crohn's disease (CD), Ulcerative colitis (UC) or both. (Especially in UC samples the lncRNAs INFG-AS1 and BC012900 were found to be significantly up-regulated. Similarly, ANRIL, a lncRNA that nest different disease associated SNPs, is significantly down-regulated in inflamed IBD tissue.) This review aims at recording for the first time recent data about lncRNAs found to be deregulated in IBDs and discussing suggestive pathogenetic mechanisms and future use of lncRNAs as biomarkers.

Keywords: Biomarker; Biopsies; Crohn’s disease; IBD genetics; Inflammatory bowel disease; Long non-coding RNAs; Plasma; Ulcerative colitis.

Publication types

  • Review

MeSH terms

  • Colitis, Ulcerative / genetics*
  • Crohn Disease / genetics*
  • Gene Expression Regulation
  • Genetic Loci
  • Humans
  • Polymorphism, Single Nucleotide
  • RNA, Long Noncoding / genetics*

Substances

  • RNA, Long Noncoding