Abstract
Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease. MicroRNAs (miRNAs) are a group of endogenous small non‑coding RNAs that regulate target genes, and play a critical role in many biological processes. However, the underlying mechanism of specific miRNA, miR‑130a‑3p, in AS remains largely unknown. Therefore, the present study aimed to explore the underlying mechanism of miR‑130a‑3p in the development of AS. In the present study, it was revealed that miR‑130a‑3p was downregulated in T cells from HLA‑B27‑positive AS patients compared with the HLA‑B27‑negative healthy controls. Next, bioinformatics software TargetScan 7.2 was used to predict the target genes of miR‑130a‑3p, and a luciferase reporter assay indicated that HOXB1 was the direct target gene of miR‑130a‑3p. Furthermore, it was determined that HOXB1 expression was upregulated in T cells from HLA‑B27‑positive AS patients. In addition, the results of the present study indicated that miR‑130a‑3p inhibitor significantly inhibited cell proliferation ability and induced cell apoptosis of Jurkat T cells, while the miR‑130a‑3p mimic promoted proliferation ability and inhibited cell apoptosis of Jurkat T cells. Notably, all the effects of the miR‑130a‑3p mimic on Jurkat T cells were reversed by HOXB1‑plasmid. Collectively, our data indicated that miR‑130a‑3p was decreased in T cells from AS patients and it could regulate T‑cell survival by targeting HOXB1.