Long non-coding RNA Mirt2 interacts with long non-coding RNA IFNG-AS1 to regulate ulcerative colitis.

Long non-coding RNAs (lncRNAs) Mirt2 and interferon-γ antisense RNA I (IFNG-AS1) play opposing roles in lipopolysaccharide (LPS)-induced inflammation, a key initiator of ulcerative colitis (UC). The present study aimed to analyze the potential interaction between Mirt2 and IFNG-AS1 in UC. Levels of IFNG-AS1 and Mirt2 in plasma samples from UC patients were measured using reverse transcription-quantitative PCR. Receiver operating characteristic curves were used to evaluate the diagnostic values of IFNG-AS1 and Mirt2 fr UC. The role of Mirt2 and IFNG-AS1 in colonic epithelial cell apoptosis was analyzed by cell apoptosis assay. In patients with UC, Mirt2 and IFNG-AS1 exhibited an inverse correlation, in which Mirt2 was downregulated while IFNG-AS1 was upregulated. Altered expression of IFNG-AS1 and Mirt2 separated patients with UC from healthy controls. In colonic epithelial cells, lipopolysaccharide treatment led to the downregulation of Mirt2 and the upregulation of IFNG-AS1. Furthermore, overexpression of Mirt2 in colonic epithelial cells resulted in downregulation of IFNG-AS1, and vice versa. Overexpression of Mirt2 led to a decreased rate of colonic epithelial cell apoptosis, while overexpression of IFNG-AS1 led to an increased rate of apoptosis. Moreover, IFNG-AS1 overexpression attenuated the effects of Mirt2 overexpression. Therefore, Mirt2 may interact with IFNG-AS1 during UC to participate in colonic epithelial cell apoptosis.