MicroRNA‑198 contributes to lupus nephritis progression by inhibition of phosphatase and tensin homology deleted on chromosome ten expression.

A number of short noncoding microRNAs (miRs) have been demonstrated to be highly expressed in many kidney diseases such as renal cancer and lupus nephritis (LN); however, these results have not been extensively investigated. The aim of the present study was to investigate the expression and function of miR-198 in LN based on the previous studies. miR-198 expression level in systemic lupus erythematosus (SLE) patients was determined to determine its clinicopathological significance and effect on glomerular cell proliferation. It was demonstrated that higher expression of miR-198 was observed in patients with SLE, and was correlated with disease activity. Bioinformatics prediction and luciferase assays were used to demonstrate that miR-198 could directly bind to the phosphatase and tensin homology deleted on chromosome ten (PTEN) 3 '-untranslated region. Furthermore, miR-198 overexpression reduced PTEN expression levels, while miR-198 silencing increased its expression at both the mRNA and protein level. Furthermore, there was a negative association between miR-198 and PTEN in the patients with active SLE. Thus, miR-198 may promote proliferation and contribute to SLE progression by targeting PTEN.