Circular RNA expression alterations in colon tissues of Crohn's disease patients.

Mol Med Rep

Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Inflammatory Bowel Disease Research Centre, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200001, P.R. China.

Published: May 2019

Genetic factors are crucial in the development of Crohn's disease (CD). Circular RNAs (circRNAs) are known to function as microRNA (miRNA) sponges and regulate a number of signalling pathways via circRNA‑miRNA interactions. As competing endogenous RNAs, the functions of circRNAs in CD should be investigated. In the present study, colon biopsy tissues were collected from ileocolon (L3)‑active CD patients and healthy controls. circRNA microarrays were performed with colon tissues from 3 CD patients and 3 controls. Subsequently, the candidate circRNAs were verified via reverse transcription‑quantitative polymerase chain reaction using colon tissues from a further 10 CD patients and 10 controls. Targeted miRNAs, genes and pathways of candidate circRNAs were predicted and analysed. Arraystar circRNA microarrays demonstrated that there were 163 upregulated circRNAs targeting 435 miRNAs and 55 downregulated circRNAs targeting 207 miRNAs (fold‑change >2 and P<0.01) in CD patients. As a candidate circRNA, hsa‑circRNA‑102685 was observed to putatively target hsa‑miR‑146b‑5p, hsa‑miR‑182‑5p and hsa‑miR‑146a‑5p. Furthermore, Kyoto Encyclopaedia of Genes and Genomes pathway analysis predicted that hsa‑circRNA‑102685 potentially participated in apoptosis, and in the Toll‑like receptor and p53 signalling pathways. Overall, the current study suggested that circRNA alterations serve an important role in the pathogenesis of CD. circRNAs, such as hsa‑circRNA‑102685, are involved in certain important signalling pathways of CD, and may be novel targets for diagnosis or treatment in this disease.

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Source
http://dx.doi.org/10.3892/mmr.2019.10070DOI Listing

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