The miR-200 family is increased in dysplastic lesions in ulcerative colitis patients

PLoS One. 2017 Mar 13;12(3):e0173664. doi: 10.1371/journal.pone.0173664. eCollection 2017.

Abstract

Background: Colorectal cancer (CRC) is a life-threatening complication of ulcerative colitis (UC), and patients are routinely screened for the development of precancerous lesions (dysplasia). However, rates of CRC development in patients with confirmed low-grade dysplasia vary widely between studies, suggesting a large degree of heterogeneity between these lesions that is not detectable macroscopically. A better understanding of the underlying molecular changes that occur in dysplasia will help to identify lesions at higher risk of malignancy. MicroRNAs (miRNAs) post-transcriptionally regulate protein expression and cell-signalling networks. Aberrant miRNA expression is a feature of sporadic CRC but much less is known about the changes that occur in dysplasia and in UC.

Methods: Comprehensive microRNA profiling was performed on RNA extracted from UC dysplastic lesions (n = 7) and UC controls (n = 10). The expression of miRNAs in UC post inflammatory polyps (n = 7) was also assessed. Candidate miRNAs were further validated by qPCR, and miRNA in situ hybridization. Serum levels of miRNAs were also assessed with a view to identification of non-invasive biomarkers of dysplasia.

Results: UC dysplasia was associated with a shift in miRNA expression profiles that was not seen in inflammatory polyps. In particular, levels of miR-200b-3p were increased in dysplasia, and this miRNA was localised to epithelial cells in dysplastic lesions and in UC cancers. No changes in miRNA levels were detected in the serum.

Conclusion: UC-Dysplasia is linked to altered miRNA expression in the mucosa and elevated miR-200b-3p levels.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Biopsy
  • Case-Control Studies
  • Colitis, Ulcerative / genetics*
  • Colitis, Ulcerative / pathology*
  • Colonic Polyps / genetics
  • Colonic Polyps / pathology
  • Female
  • Gene Expression Regulation
  • Genetic Markers
  • Humans
  • Inflammatory Bowel Diseases / genetics
  • Inflammatory Bowel Diseases / pathology
  • Male
  • MicroRNAs / blood
  • MicroRNAs / genetics*
  • Middle Aged
  • Real-Time Polymerase Chain Reaction
  • Reproducibility of Results

Substances

  • Genetic Markers
  • MIRN200 microRNA, human
  • MicroRNAs

Grants and funding

This work was supported by the Broad Medical Research Program of the Broad Foundation [http://www.ccfa.org/science-and-professionals/broad/] (grant no IBD-0289R to Professor Silver and Dr James Lindsay) and Barts and The London Charity [https://bartscharity.org.uk] (grant no MGD0016 to Noor Jawad). The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data and preparation, review, or approval of the manuscript.