Elevated expression of ciRS-7 in peripheral blood mononuclear cells from rheumatoid arthritis patients

• প্রধান লেখক: Xinyi Tang (লেখক), Jiemin Wang (লেখক), Xin Xia (লেখক), Jie Tian (লেখক), Ke Rui (লেখক), Huaxi Xu (লেখক), Shengjun Wang (লেখক)
• বিন্যাস: গ্রন্থ
• প্রকাশিত: BMC, 2019-02-01T00:00:00Z.
• বিষয়গুলি: article
• অনলাইন ব্যবহার করুন: Connect to this object online.
• Notes: 10.1186/s13000-019-0783-7; 1746-1596
• Keywords: ciRS-7; miR-7; mTOR; Rheumatoid arthritis; Pathology; RB1-214
• Source: Diagnostic Pathology, Vol 14, Iss 1, Pp 1-6 (2019)

Abstract Background Circular RNAs (circRNAs) represent a class of widespread and variety endogenous RNAs that may regulate gene expression. Thousands of mammalian circRNAs harbor miRNA response elements (MREs), suggesting a potential role as competitive endogenous RNAs (ceRNAs). Recent studies have demonstrated that ciRS-7 (circular CDR1 antisense), which acts as a powerful miR-7 sponge, contains more than 70 putative binding sites for miR-7 and may inhibit its target genes. The aim of this preliminary study was to investigate the expression of ciRS-7 in patients with rheumatoid arthritis (RA) as well as the correlation between ciRS-7 and the target genes of miR-7. Methods Eighteen patients with RA and 14 healthy controls were enrolled in the current study. The relative expression of ciRS-7, miR-7, miR-671 and mTOR in peripheral blood mononuclear cells (PBMCs) from these samples were detected by real-time PCR. Results We found that ciRS-7 was significantly increased in RA patients and could potentially differentiate the RA patients from healthy controls. Additionally, the expression of mTOR, one of the miR-7 target genes, had positive and negative relationships with ciRS-7 and miR-7 expression, respectively. Notably, the relative expression of miR-671, which mediated the regulation of circular CDR1 antisense homeostasis, was significantly decreased in RA patients. Conlusion Downregulated miR-671 may influence the level of ciRS-7 in RA patients. Enhanced ciRS-7 could inhibit the function of miR-7 and further relieve the inhibitory effect of miR-7 on mTOR.